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Neuroscience Researcher Biographical Sketches and Research Summaries [1 ed.]
 9781621009801, 9781621009436

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Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

NEUROSCIENCE RESEARCH PROGRESS

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

NEUROSCIENCE RESEARCHER BIOGRAPHICAL SKETCHES AND RESEARCH SUMMARIES

No part of this digital document may be reproduced, stored in a retrieval system or transmitted in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

NEUROSCIENCE RESEARCH PROGRESS

NEUROSCIENCE RESEARCHER BIOGRAPHICAL SKETCHES AND RESEARCH SUMMARIES ABRAM A. CHERNYOVSKAYA AND

GRAVIIL F. KLOSSOVSKY Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

EDITORS

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Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2013 by Nova Science Publishers, Inc. All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers‘ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works.

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

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Published by Nova Science Publishers, Inc. † New York Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

CONTENTS

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Preface

xix

Part 1 - Research Biographies

1

Chapter 1

Biographical Sketch Miroslava Anderova

3

Chapter 2

Biographical Sketch Richard A. Armstrong

7

Chapter 3

Biographical Sketch Haruhiko Banno

11

Chapter 4

Biographical Sketch Alfred Bennun

13

Chapter 5

Biographical Sketch Kim M. Cecil

17

Chapter 6

Biographical Sketch Malka Cohen-Armon

21

Chapter 7

Biographical Sketch Paola De Bartolo

25

Chapter 8

Biographical Sketch Valentina Echeverria

29

Chapter 9

Biographical Sketch Sebastiaan Engelborghs

39

Chapter 10

Biographical Sketch Carl L. Faingold

41

Chapter 11

Biographical Sketch Alon Friedman

45

Chapter 12

Biographical Sketch Valantis Fyndanis

49

Chapter 13

Biographical Sketch Rigoberto Gonzalez Pina

51

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Contents

vi Chapter 14

Biographical Sketch Sunghoi Hong

53

Chapter 15

Biographical Sketch Kazuaki Inoue

57

Chapter 16

Biographical Sketch Felix Junyent Herena

61

Chapter 17

Biographical Sketch Anna Hrabovska

65

Chapter 18

Biographical Sketch Masahisa Katsuno

69

Biographical Sketch Michelle Y. Kibby

71

Chapter 20

Biographical Sketch Philip C. Ko

73

Chapter 21

Biographical Sketch Keith R. Laws

75

Chapter 22

Biographical Sketch Iscia Lopes-Cendes

79

Chapter 23

Biographical Sketch Paul R. Martin

83

Chapter 24

Biographical Sketch Martin H. Maurer

87

Chapter 25

Biographical Sketch Eiji Nakagawa

91

Chapter 26

Biographical Sketch Takehiko Nakama

93

Chapter 27

Biographical Sketch J. Patrick Neary

97

Chapter 28

Biographical Sketch Kirill Nikolayevich Dudkin

99

Chapter 29

Biographical Sketch Alan M. Palmer

101

Chapter 30

Biographical Sketch José Miguel Pêgo

103

Chapter 31

Biographical Sketch Pessia Mauro

107

Chapter 32

Biographical Sketch Joseph P. Pillion

111

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chapter 19

.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Contents

vii

Chapter 33

Biographical Sketch Quercioli Alessandra

115

Chapter 34

Biographical Sketch M. Dominique Sappey-Marinier

117

Chapter 35

Biographical Sketch Hans-Georg Schlosser

121

Chapter 36

Biographical Sketch Nobuaki Shimoda

123

Chapter 37

Biographical Sketch Tetsuya Shimokawa

125

Chapter 38

Biographical Sketch Amruthesh C. Shivachar

127

Chapter 39

Biographical Sketch Gen Sobue

129

Chapter 40

Biographical Sketch Keisuke Suzuki

131

Chapter 41

Biographical Sketch Feng Ru Tang

133

Chapter 42

Biographical Sketch Maria Victoria Tejada-Simon

137

Chapter 43

Biographical Sketch Stefan Van der Mussele

141

Chapter 44

Biographical Sketch Brankica Vasiljevic

143

Chapter 45

Biographical Sketch Viroj Wiwanitkit

147

Chapter 46

Biographical Sketch Jiann-Ming Wu

149

Chapter 47

Biographical Sketch Wandong Zhang

151

Part 2 - Research Summaries in Neuroscience Chapter 48

A System Architecture Approach to the Brain: From Neurons to Consciousness L. Andrew Coward

155 157

Chapter 49

Adaptive Mechanisms in Migraine Vinod Kumar Gupta

159

Chapter 50

Another View of the Brain System Toshifumi Kumai and Shibukawa Yoshiyuki

161

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

viii Chapter 51

Chapter 52

Basal Ganglia and Thalamus: Their Role in Cognition and Behaviour Rita Moretti, Paola Torre and Rodolfo M. Antonello

163

Biogenic Amines: Pharmacological, Neurochemical and Molecular Aspects in the CNS Tahira Farooqui and Akhlaq A. Farooqui

165

Chapter 53

Brain and Dissociated Mind Petr Bob

167

Chapter 54

Cerebral Blood Flow Regulation Nodar P. Mitagvaria and Haim (James) I. Bicher

169

Chapter 55

Cerebral Ischemia in Young Adults: Pathogenic and Clinical Perspectives Alessandro Pezzini and Alessandro Padovani

171

Chapter 56

Cognitive Impairment in Children with ADHD Alasdair Vance, Catherine Mollica and Paul Maruff

173

Chapter 57

Cognitive Visual Memory in Cats V. M. Okujava and T. A. Natishvili

175

Chapter 58

Cognitive-Behavioral and Neuropsychological Models of Obsessive-Compulsive Disorder Claudio Sica, Luigi Rocco Chiri, Dean McKay and Marta Ghisi

Chapter 59 Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Contents

Chapter 60

177

Cultural and Linguistic Influence on Developmental Neural Basis of Theory of Mind: Whorfian Hypothesis Revisited Chiyoko Kobayashi Frank

179

Developmental Neurotoxicity of PBDEs, Mechanisms and Implications Henrik Alm and Birger Scholz

181

Chapter 61

Electromagnetic Mind Control: Fact or Fiction? A Scientific View V. N. Binhi

183

Chapter 62

Experimental Animal Models in Neurobehavioral Research Allan V. Kalueff and Justin L. LaPorte

185

Chapter 63

Isoflavones: A Race after the Rescue of the Aging Hippocampus Catherine Bennetau-Pelissero, Khalid Jamali and Aline Marighetto

187

Chapter 64

Multiple Facets of Anger: Getting Mad or Restoring Justice? Farzaneh Pahlavan

189

Chapter 65

Neuroplasticity Following Skill and Strength Training Alan J. Pearce and Dawson J. Kidgell

191

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Contents

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chapter 66

Neuroplasticity in the Auditory Brainstem: From Physiology to the Drug Therapy Angelo Salami

ix

193

Chapter 67

Neuroscience in the Age of Complexity Franco F. Orsucci and Nicoletta Sala

195

Chapter 68

Neurosciences in Music Pedagogy Frances Rauscher and Wilfried Gruhn

197

Chapter 69

Society, Behaviour and Epilepsy Jaya Pinikahana and Christine Walker

199

Chapter 70

Symbiotic Biofilms and Brain Neurochemistry Alexander V. Oleskin, Vladimir I. Shishov and Kristina Malikina

201

Chapter 71

Working Memory in Infants Jing Sun and Nicholas Buys

203

Chapter 72

Neural Signal Estimation through Time-Resolved Functional Imaging C. W. Tyler and L. T. Likova

Chapter 73

DNA Damage Response and Apoptosis of Postmitotic Neurons Inna I. Kruman and Elena I. Schwartz

Chapter 74

Hallmarks of Apoptotic-Like Cell Death in Response to Hypoxic Injury in Various Developmental Models Are Closely Related to Brain Immaturity Jean-Luc Daval and Christiane Charriaut-Marlangue

Chapter 75

Chapter 76

Chapter 77

Chapter 78

Chapter 79

205 207

209

The Use of Neural Stem Cells in Treating Traumatic Brain Injury in Rats Shu-Yuan Yang and Hui Liu

211

Subdural Interictal EEG Analysis for Extracting Discriminating Features towards Electrode Classification Using Artificial Neural Networks Mercedes Cabrerizo, Malek Adjouadi, Melvin Ayala and Prasanna Jayakar

213

Laboratory Memory Tasks and Autobiographical Recollection: Cognitive and Neurofunctional Evidence for Differential Forms of Episodic Memory Martina Piefke Brain Electric Source Imaging by an Iterative Correlation Matrix Based Multiple Signal Classification Approach Dezhong Yao Mapping of Brain Operational Architectonics Andrew A. Fingelkurts and Alexander A. Fingelkurts

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

215

217 219

x Chapter 80

Neural Mechanisms in Anxiety and Panic Marcus Lira Brandão and Julia Maria dos Santos

Chapter 81

Phase Synchronization at Different Frequency Bands Induced by the Emotional Film Stimuli of Happiness, Sadness and Fear Tommaso Costa, Elena Rognoni, Dario Galati and Manuella Crini

Chapter 82

Cognitive Aspects in Idiopathic Epilepsy Sherifa A. Hamed

Chapter 83

Cognitive Impairment in Children with ADHD: Developing a Novel Standardised Single Case Design Approach to Assessing Stimulant Medication Response Catherine Mollica, Paul Maruff and Alasdair Vance

Chapter 84

Novel Therapies for Alzheimer's Disease: Potentially Disease Modifying Drugs Daniela Galimberti, Chiara Fenoglio and Elio Scarpini

221

223 225

227

229

Chapter 85

Cognitive Interventions to Improve Prefrontal Functions Yoshiyuki Tachibana, Yuko Akitsuki and Ryuta Kawashima

Chapter 86

Insights from Proteomics into Mild Cognitive Impairment, Likely the Earliest Stage of Alzheimer‘s Disease Renã A. Sowell and D. Allan Butterfield

233

Animal Models for Cerebrovascular Impairment and its Relevance in Vascular Dementia Veronica Lifshitz and Dan Frenkel

235

The Critical Role of Cognitive Function in the Effective Selfadministration of Inhaler Therapy S. C. Allen

237

Foetal Alcohol Spectrum Disorders: The 21st Century Intellectual Disability Teresa Whitehurst

239

Where There are no Tests: A Systematic Approach to Test Adaptation Penny Holding, Amina Abubakar and Patricia Kitsao Wekulo

241

Paid Personal Assistance for Older Adults with Cognitive Impairment Living at Home: Current Concerns and Challenges for the Future Claudio Bilotta, Luigi Bergamaschini, Paola Nicolini and Carlo Vergani

243

Chapter 87

Chapter 88 Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Contents

Chapter 89

Chapter 90

Chapter 91

Chapter 92

Neurotoxicity, Autism, and Cognitive Impairment Rebecca Cicha, Brett Holfeld and F. R. Ferraro

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

231

245

Contents Chapter 93

Chapter 94

Chapter 95

Chapter 96

Chapter 97

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chapter 98

Common Questions and Answers to Deep Brain Stimulation Surgery Fernando Seijo, Marco Alvarez-Vega, Beatriz Lozano, Fernando Fernández-González, Elena Santamarta and Antonio Saíz Deep Brain Stimulation and Cortical Stimulation Methods: A Commentary on Established Applications and Expected Developments Damianos E. Sakas and Ioannis G. Panourias Cortical Stimulation versus Deep Brain Stimulation in Neurological and Psychiatric Disorders: Current State and Future Prospects Damianos E. Sakas and Ioannis G. Panourias Invasive Cortical Stimulation for Parkinson‘s Disease and Movement Disorders B. Cioni, A. R. Bentivoglio, C. De Simone, A. Fasano, C. Piano, D. Policicchio V. Perotti and M. Meglio Deep Brain Stimulation in Epilepsy: Experimental and Clinical Data M. Langlois, S. Saillet, B. Feddersen, L. Minotti, L. Vercueil, S Chabardès, O. David, A. Depaulis, P. Kahane and C. Deransart Psychosurgery of Obsessive-Compulsive Disorder: A New Indication for Deep Brain Stimulation? Dominique Guehl, Abdelhamid Benazzouz, Bernard Bioulac, Pierre Burbaud, Emmanuel Cuny, Alain Rougier, Jean Tignol, and runo Aouizerate

Chapter 99

Deep Brain Stimulation in Adult and Pediatric Dystonia Laura Cif, Simone Hemm, Nathalie Vayssiere and Philippe Coubes

Chapter 100

Deep Brain Stimulation of the Subthalamus: Neuropsychological Effects Rita Moretti, Paola Torre, Rodolfo M. Antonello and Antonio Bava

Chapter 101

Chapter 102

Subthalamic High-Frequency Deep Brain Stimulation Evaluated by Positron Emission Tomography in a Porcine Parkinson Model Mette S. Nielsen, Flemming Andersen, Paul Cumming, Arne Møller, Albert Gjedde, Jens. C. Sørensen and Carsten R. Bjarkam Current and Future Perspectives on Vagus Nerve Stimulation in Treatment-Resistant Depression Bernardo Dell’Osso, Giulia Camuri, Lucio Oldani and A. Carlo Altamura

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

xi

247

249

251

253

255

257

259

261

263

265

xii Chapter 103

Interhemispheric Connectivity: The Evolution and Nature of the Corpus Callosum Sarah B. Johnson and Manuel F. Casanova

Chapter 104

White Matter Lesions: From Present to Future R. P. W. Rouhl, R. J. van Oostenbrugge and J. Lodder

Chapter 105

White Matter Lesions and Aging in HIV Infection: Implications for Development of Cognitive Decline and Dementia Aaron M. McMurtray, Beau Nakamoto, Kalpana Kallianpur and Erin P. Saito

267 269

271

Chapter 106

White Matter Changes in Drug Abuse and in HIV-1 Infection Andreas Büttner, Jeremias Wohlschaeger, Ida C. Llenos and Serge Weis

273

Chapter 107

White Matter Changes in Critical Illness and Delirium Max L. Gunther, Carlos Faracoand Alessandro Morandi

275

Chapter 108

White Matter Involvement in Neuromuscular Disorders Petr Vondracek, Marketa Hermanova, Kristina Vodickova, Lenka Fajkusova, Eva Brichtováand Jarmila Skotakova

277

Chapter 109

White Matter Hyperintensities in Psychiatric Disorders and Their Association with Suicide Risk Maurizio Pompili, Gianluca Serafini, Silvia Rigucci, Andrea Romano, Marco Innamorati, Antonio Del Casale, Daniela Di Cosimo, Roberto Tatarelli and David Lester

Chapter 110 Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Contents

A Quantitative Study of the Pathological Changes in the Cortical White Matter in Variant Creutzfeldt-Jakob Disease (vCJD) Richard A. Armstrong

279

281

Chapter 111

Progressive Multifocal Leukoencephalopathy Endre Pál

Chapter 112

Remyelination Failure in Multiple Sclerosis and Vulnerability of Oligodendrocytes to Repeated Insults Catherine Fressinaud

285

Endoscopic Anatomy of the Thecal Sac Using a Flexible Steerable Endoscope Jan Peter Warnke

287

Chapter 113

Chapter 114

White Matter Abnormalities in the Diabetic-Hypertensive Brain Natalia Rinconand Cory Toth

Chapter 115

Brain Tissue Segmentation Based on Multi-Channel Diffusion Tensor Imaging Data Tianming Liuand Stephen T. C. Wong

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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289

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Contents Chapter 116

Chapter 117

Chapter 118

Origin and Function of Amoeboid Microgliai Cells in the Periventricular White Matter in the Developing Brain C. Kaur and E. A. Ling Diffusion Tensor Imaging Is More Sensitive than Conventional Magnetic Resonance Imaging in Demonstrating White Matter Abnormalities in Susac's Syndrome Ilka Kleffner, Michael Deppe, Siawoosh Mohammadi, Philip Van Damme, Stefan Sunaert, Wolfram Schwindt, Jens Sommer, Peter Young and E. B. Ringelstein

293

295

297

Chapter 119

Organisation of the Node of Ranvier in Myelinated Central Axons James J. P. Alix

Chapter 120

Organizing Principles of Projections of the Long Descending Reticulospinal Pathways and Their Targets‘ Spinal Commissural Neurons: With Special Reference to the Locomotor Function Kiyoji Matsuyama,, and Kaoru Takakusaki

301

Diffusion Tensor MRI Data Acquisition Methods for White Matter and Clinical Applications: Non Echo-Planar Imaging Masaaki Hori

303

Chapter 121

Chapter 122 Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Three-Dimensional Microstructural Analysis of Human Brain Tissue by Using Synchrotron Radiation Microtomographs Ryuta Mizutani, Akihisa Takeuchi, Kentaro Uesugi, Susumu Takekoshi, R. Yoshiyuki Osamura and Yoshio Suzuki

xiii

Chapter 123

Chapter 124

Chapter 125

Chapter 126

The Dimensions of the Sacral Spinal Canal in Thecaloscopy: A Morphometric MRI Study S. Mourgela, A. Sakellaropoulos, S. Anagnostopoulou and J. P. Warnke Cocaine's Impact on Affect, Activity, and Reward Are DoseDependently Impacted by Age: Adolescent Versus Adult Exposure Brian M. Kelley, Candace E. Perry, Hillary A. Hershey and Adrianna L. Baird Meeting Adolescents Where They Are, Literally and Figuratively: Embracing Emerging Persuasive Technologies for Tobacco Cessation Treatment Brian M. Kelley

299

305

307

309

An Exploration of Human Swallowing Using Transcranial Magnetic Stimulation and Other Non-Invasive Technologies S. Mistry, E. Michou, V. Jayasekeran and S. Hamdy

311

Transcranial Magnetic Stimulation and the Human Neuromuscular System Marisa P. McGinley and Brian C. Clark

313

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

xiv Chapter 127

Chapter 128

rTMS Treatment of Depression: Current Status and Future Directions Paul B. Fitzgerald Animal Models of Alzheimer Disease for Translational Research: Current and Future Concepts Shuko Takeda, Naoyuki Sato, Hiromi Rakugi and Ryuichi Morishita

315

317

Chapter 129

Enhancement Strategies for TMS Effects in Tinnitus Treatment Tobias Kleinjung and Berthold Langguth

319

Chapter 130

Tinnitus and Transcranial Magnetic Stimulation (TMS) Berthold Langguth and Tobias Kleinjung

321

Chapter 131

Music and Concepts Jérôme Daltrozzo, Jean Vion-Dury and Daniele Schön

323

Chapter 132

Molecular Mechanisms Involved in the Pathogenesis of Huntington Disease Claudia Perandones, Martín Radrizzani and Federico Eduardo Micheli

Chapter 133

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Contents

Huntingtin Interacting Proteins: Involvement in Diverse Molecular Functions, Biological Processes and Pathways Nitai P. Bhattacharyya, Moumita Datta, Manisha Banerjee, Srijit Das and Saikat Mukhopadhyay

Chapter 134

DNA Repair and Huntington's Disease Fabio Coppedè

Chapter 135

Putting Together Evidence and Experience: Best Care in Huntington‘s Disease Zinzi Paola, Jacopini Gioia, Frontali Marinaand Bentivoglio and Anna Rita

325

327

329

331

Chapter 136

Oral Health Care for the Individual with Huntington‘s Disease Robert Rada

333

Chapter 137

Suicidal Ideation and Behaviour in Huntington‘s Disease Tarja-Brita Robins Wahlin

335

Chapter 138

Making Reproductive Decisions in the Face of a Late-Onset Genetic Disorder, Huntington‘s Disease: An Evaluation of Naturalistic Decision-Making Initiatives Claudia Downing

Chapter 139

The Control of Adult Neurogenesis by the Microenvironment and How This May Be Altered in Huntington‘s Disease Wendy Phillips and Roger A. Barker

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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339

Contents Chapter 140

341

Chapter 141

Life Skills Instruction in a Time of Accountability Beth Ackerman and Katherine Quigley

343

Chapter 142

Pro-Inflammatory Cytokines in Learning and Memory Amaicha Mara Depino

345

Chapter 143

Perceptions of Forgetfulness in Adulthood: Does Memory Knowledge Matter? Susan Brigman and Katie E. Cherry

347

Memory Reconsolidation: History, Research, and Implications for Treatment of Psychiatric Disorders Robert W. Flint, Jr., Karina H. Bengsz and Aeron E. Zamecnik

349

Chapter 144

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Emotion‘s Effects on Attention and Memory: Relevance to Posttraumatic Stress Disorder Katherine Mickley Steinmetz and Elizabeth Kensinger

xv

Chapter 145

Intellectual Disability: Beyond IQ Scores Nahal Goharpey, David P. Crewther and Sheila G. Crewther

Chapter 146

Facilitatory Effects of Music on Memory: A Review of the Potential Role of Emotional Arousal Sherilene M. Carr and Nikki S. Rickard

Chapter 147

Spatial Memory and Large-Scale Ecological Environments Tina Iachini, Gennaro Ruggiero and Francesco Ruotolo

Chapter 148

Does Disregard of Transient Changes in the Environment Differentiate Behaviour of Children with Autism from Typically Developing Children and those with Down Syndrome and Idiopathic Intellectual Disability? Nahal Goharpey, Robin Laycock, David P. Crewther and Sheila G. Crewther

Chapter 149

Studying Memory: From the Frontal to the Temporal Lobe and Vice-Versa Orlando Francisco Amodeo Bueno

Chapter 150

Learning Deficits in Presenilin Mutant Mice R. Lalonde and C. Strazielle

Chapter 151

Assessing Alertness in Children with Profound Intellectual and Multiple Disabilities Carla Vlaskamp and Vera Munde

Chapter 152

Chapter 153

Assessment of Time Processing Ability and Daily Time Management in Children with and Without Developmental Disabilities Gunnel Janeslätt, Mats Granlund and Anders Kottorp A Geography of Intellectual Disabilities Andrew Power

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

351

353 355

357

359 361

363

365 367

xvi Chapter 154

Chapter 155

Chapter 156

Chapter 157

Chapter 158

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chapter 159

Contents Prefrontal Morphology, Neurobiology and Clinical Manifestations of Schizophrenia Tomáš Kašpárek

369

Prefrontal Cholinergic Receptors: Their Role in the Pathology of Schizophrenia M. Udawela, E. Scarr and B. Dean

371

The Interrelationship between Dopamine and Noradrenaline in the Prefrontal Cortex: From Physiology to Therapy Ezio Carboni and Anna Rosa Carta

373

Participation of the Prefrontal Cortex in the Processing of Sexual and Maternal Incentives Marisela Hernández González and Miguel Angel Guevara

375

From Conflict to Problem Solution: The Role of the Medial Prefrontal Cortexin the Learning of Memory-Guidedand ContextAdequate Behavioral Strategies for Problem-Solving in Gerbils Holger Stark The Orbitofrontal Cortex and Emotional Decision-Making: The Neglected Role of Anxiety Sabine Windmann and Martina Kirsch

Chapter 160

PEEF: Premotor Ear-Eye Field. A New Vista of Area 8B Bon Leopoldo, Marco Lanzilotto and Cristina Lucchetti

Chapter 161

Prefrontal Cortex: Its Roles in Cognitive Impairment in Parkinson‘s Disease Revealed by PET Qing Wangab, Kelly A. Newella, Peter T. H. Wongd and Ying Luc

377

379 381

383

Chapter 162

Noradrenergic Actions in Prefrontal Cortex: Relevance to AD/HD Amy F. T. Arnsten

385

Chapter 163

Prefrontal Cortex: Brodmann and Cajal Revisited Guy N. Elston and Laurence J. Garey

387

Chapter 164

Developmental Characteristics in Category Generation Reflects Differential Prefrontal Cortex Maturation Julio Cesar Flores Lázaro and Feggy Ostrosky-Solís

389

Chapter 165

Working Memory and the Autistic Mind R. Hansen, L. Deling, E. Olufs, R. Pytlik and F. R. Ferraro

391

Chapter 166

Measurement of Working Memory Karlee D. Fellner and John R. Reddon

393

Chapter 167

Effects of Visuo-Spatial Working Memory on Wayfinding Ability Laura Piccardi and Raffaella Nori

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

395

Contents Chapter 168

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chapter 169

xvii

Working Memory and Prefrontal Cortex and Their Relation with the Brain Reward System and Drug Addiction Ester Miyuki Nakamura-Palacios

397

Working Memory in the Service of Verbal Episodic Encoding: A Cognitive Neuropsychological Perspective Matthew J. Wright, Peter Bachman and Ellen Woo

399

Chapter 170

Working Memory in Preterm and Full-Term Infants Jing Sun and Nicholas Buys

Chapter 171

The Assessment and Training of Working Memory for Prevention and Early Intervention in Case of Reading, Writing and Arithmetical Difficulties in Children Antonella D’Amico

Chapter 172

Working Memory in Sentence Comprehension and Production Matthew J. Traxler, David Caplan, Debra L. Long and Gloria S. Waters

Chapter 173

Working Memory Components and Virtual Reorientation: A Dual-Task Study Alessandro O. Caffò, Luciana Picucci, Manuela N. Di Masi and Andrea Bosco

401

403 405

407

Chapter 174

Using fMRI to Examine the Brain: Bases of Working Memory Michael A. Motes, Ehsan Shokri Kojori, Neena K. Rao, Ilana J. Bennett and Bart Rypma

Chapter 175

Aging and Short-Term Memory for Face Identity of Emotional Faces Sandra J. E. Langeslag and Jan W. van Strien

411

Varying Background Colours Reveals that Enhanced Short-Term Memory for Angry Faces Is a Valence and Not an Arousal Effect Sandra J. E. Langeslag, Margaret C. Jackson, Jan W. van Strien and David E. J. Linden

413

Working Memory Deficits in Schizophrenia: Neurobiological Correlates and Treatment Haiyun Xu, Hong-Ju Yang and Gregory M. Rose

415

Tobacco, Nicotine and Cotinine: For Memory, Neurological, and Psychiatric Disorders V. Echeverria, P. Rajeev and R. Zeitlin

417

Working Memory and Functional Outcome in Patients with Major Depressive Disorder Yasuhiro Kaneda

419

Chapter 176

Chapter 177

Chapter 178

Chapter 179

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Contents

xviii Chapter 180

Control of Working memory Contents During Task-Switching James A. Grange

421

Chapter 181

Development of Neural Mechanisms of Working Memory V. Vuontela and S. Carlson

423

Chapter 182

Molecular Imaging B. Schaller and N. Sandu

425

Chapter 183

MRI Measurement of Fornix Pathology: Evidence of Extensive Fornix Damage Following Surgical Removal of Colloid Cysts in the Third Ventricle John P. Aggleton, Andrew R. Mayes, Vanessa Sluming, Neil Roberts and Daniela Montaldi

427

Sudden Intrauterine Unexplained Death (SUD) ―Gray Zone‖ or Borderline Giulia Ottaviani

429

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Chapter 184

Chapter 185

Neuroimaging of the Fornix: Present and Future Christine E. Denby, Seralynne D. Vann, Dimitris Tsivilis, Andrew R. Mayes, Daniela Montaldi and John P. Aggleton

431

Chapter 186

High-Field MR Imaging in Neuroscience Research N. R. Jagannathan

433

Chapter 187

Perioperative Atrial Fibrillation and the Risk of Stroke Maciej Banach and Jacek Rysz

435

Chapter 188

Mini-Review: Ethics in Neuroscience Bernhard Schaller

437

Chapter 189

The Functional Neuroimaging of the Precuneus Andrea E. Cavanna, Luca Bertero and Stefano L. Cavanna

439

Chapter 190

Link between Basic and Clinical Research by Functional Imaging Bernhard J. Schaller

441

Chapter 191

Extended Expression for Transverse Magnetization Using Four Pulse Sequence to Construct Double Quantum Filter of Arbitrary Phases for Spin 3/2 Sodium Nuclei Rakesh Sharma

Chapter 192

Chapter 193

MALDI Imaging: A Review of the Current Status of the Technology Isabelle Fournier, Franck Julien, Maxence Wisztorski, Eduardo Macagno and Michel Salzet Imaging in Molecular Dynamics: Technology and Applications Benjamin Whitaker

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445

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PREFACE

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This new book compiles biographical sketches of top professionals in the field of neurosciences, as well as research summaries from a number of different focuses in this important field.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

PART 1 - RESEARCH BIOGRAPHIES

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 1

BIOGRAPHICAL SKETCH Miroslava Anderova Title: Dpt. of Cellular Neurophysiology, Institute of Experimental medicine ASCR, Prague, Czech Republic

Date of Birth: 4.4.1958

EDUCATION Institution and Location

Degree

Year Conferred

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PhD

Scientific Field Microbiology and Molecular Genetics

Contact points Videnska 1083, Prague 4-Krc, 142 20, Czech Republic

RESEARCH AND PROFESSIONAL EXPERIENCE The role of glial cells in CNS pathologies and CNS repair/regeneration

Professional Appointments 1991-1993: Postdoctoral position Department of Biology, UCSD San Diego, USA 1993-1995: Postdoctoral position Dept. of Pharmacology, University Loui Pasteur, Strasbourg, France 1997: Research scientist Department of Neuroscience, Institute of Experimental Medicine ASCR, Prague, Czech Republic Institute of Experimental Medicine ASCR

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Abram A. Chernyovskaya and Graviil F. Klossovsky

2007-2008: Research scientist Department of Cellular Neurophysiology, Institute of Experimental Medicine ASCR, Prague, Czech Republic 2009-2010: Head of Laboratory Department of Cellular Neurophysiology, Laboratory of Neurobiology, Institute of Experimental Medicine ASCR, Prague, Czech Republic 2010: Head of Department Department of Cellular Neurophysiology, Laboratory of Neurobiology, Institute of Experimental Medicine ASCR, Prague, Czech Republic

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Publications during last three years 1. Prajerova, I., Honsa, P., Chvatal, A., Anderova, M. (2010): Distinct effects of Sonic hedgehog and Wnt-7a on differentiation of neonatal neural stem/progenitor cells in vitro. Neuroscience, 15;171(3): 693-711, IF 3.2 2. Anderova M, Vorisek I, Pivonkova H, Benesova J, Vargova L, Cicanic M, Chvatal A, Sykova E. (2010): Cell death/proliferation and alterations in glial morphology contribute to changes in diffusivity in the rat hippocampus after hypoxia/ischemia. JCBFM 31, 894907, IF 5.457 3. Pivonkova H, Benesova J, Butenko O, Chvatal A, Anderova M.(2010): Impact of Global Cerebral Ischemia on K+ Channel Expression and Membrane Properties of Glial Cells in the Rat Hippocampus. Neurochemistry International 57(7):783-94, IF 3.541 4. Kozubenko N., Turnovcova K., Kapcalova M., Butenko O., Anderova M., Rusnakova V., Kubista M., Hampl A., Jendelova P., Sykova E. (2010) Analysis of in vitro and in vivo characteristics of human embryonic stem cell-derived neural precursors. Cell transplantation, 19(4):471-86. IF 5,251 5. Prajerova, I., Honsa, P., Chvatal, A., Anderova, M. (2009): Neural stem/progenitor cells derived from the embryonic dorsal telencephalon of D6/GFP mice differentiate primarily into neurons after 6. Verkhratsky A, Anderova M, Chvatal A. (2009): Differential calcium signaling in neuronal-glial networks. Frontiers in Bioscience 14, 2004-2016 IF 2.989 7. Vignali M, Benfenati V, Caprini M, Anderova M, Nobile M, Ferroni S (2009): The endocannabinoid anandamide inhibits potassium conductance in rat cortical astrocytes Glia 57:791–806 IF 5.599 8. Benesova J, Hock M, Butenko O, Prajerova I, Anderova M, Chvatal A. (2008): Quantification of astrocyte volume changes during ischemia in situ reveals two populations of astrocytes in the cortex of GFAP/EGFP mice J Neurosci Res. 2009 Jan;87(1):96-111. Res IF 3.096 9. Chvatal A, Anderova M, Neprasova H, Prajerova I, Benesova J, Butenko O, Verkhratsky A. (2008): Pathological potential of astroglia. Physiol Res. IF 1.65 10. Chvatal A., Anderova M., Kirchhoff F (2007) Three-dimensional confocal morphometry a new approach for studying dynamic changes in cell morphology in brain slices. J Anat.210(6), 671-83 IF 2.458 11. Jelitai, M., Anderova, M., Chvatal, A., Madarasz, E. (2007) Electrophysiological characterization of neural stem/progenitor cells during in vitro differentiation: a study on an immortalized neuroectodermal cell line. J Neurosci Res. 85:1606-1617. IF=3.239

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Research Biographies - Miroslava Anderova

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12. Neprasova H, Anderova M, Petrik D, Vargova L, Kubinova Š, Chvatal A.a Sykova E.: (2007) Changes in voltage-dependent K+ and Na+ currents and volume regulation in astrocytes exposed to elevated K+ Pflugers Archives-453(6), 839-49. IF=3.564 13. Chvatal A., Anderova M., Hock M., Prajerová I., Neprasova H., Chvatal V., Kirchhoff F., Sykova E. (2007) Real-time three-dimensional confocal morphometry reveals structural changes in astrocyte morphology in situ. J. Neurosci. Res 78, 668-682. IF=3.239

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 2

BIOGRAPHICAL SKETCH Richard A. Armstrong Title: Aston University

Date of Birth: 25 11 1949

EDUCATION

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Institution and Location King‘s College London UK, University of Oxford

Degree

Year Conferred

Scientific Field

RESEARCH AND PROFESSIONAL EXPERIENCE Address: Dept of Vision Sciences, Aston University, Birmingham B4 7ET

Publications during last three years Armstrong RA (2009a) Pathological changes in the sporadic and variant forms of CreutzfeldtJakob disease (CJD) are spatially related to blood vessels. Brain Research Journal 2 (3) 149-162. Armstrong RA (2009b) Monthly fluctuations in radial growth of individual lobes of the lichen Parmelia conspersa (Ehrh. Ex Ach.) Ach. Symbiosis 47: 9-16. Armstrong RA (2009c) Spatial correlations between β -amyloid (A β) deposits and blood vessels in early-onset Alzheimer‘s disease. In: Alzheimer’s Disease in the Middle-Aged. Ed: Hyun Sil Jeong, Nova Science Publishers, pp 137-153. Armstrong RA (2009d) Spatial correlations between β -amyloid (A β) deposits and blood vessels in familial Alzheimer‘s disease. Folia Neuropathol 46: 241-248.

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Armstrong RA, Lantos PL, Cairns NJ (2009e) Hippocampal pathology in progressive supranuclear palsy (PS): a quantitative study of 8 cases. Clin Neuropathol 28: 46-53. Armstrong RA, Ironside JW, Lantos PL, Cairns NJ (2009f) A quantitative study of the pathological changes in the cerebellum in 15 cases of variant Creutzfeldt-Jakob disease (vCJD). Neuropathol Appl Neurobiol 35: 36-45. Armstrong RA (2009g) Relationship between the microcirculation and the pathological changes in the sporadic and variant forms of Creutzfeldt-Jakob disease (CJD). In:Microcirculation: Function, Malfunction and Measurement. Ed: Ralph Thompson, Nova Science Publishers, pp 79-94. Armstrong RA, Cairns NJ (2009h) Laminar distribution of the pathological changes in frontal and temporal cortex in 8 patients with progressive supranuclear palsy. Clin Neuropathol 28: 350-357. Armstrong RA, Cairns NJ (2009i) Clustering and spatial correlations of the neuronal cytoplasmic inclusions, astrocytic plaques and ballooned neurons in corticobasal degeneration. J Neural Transm. 116: 1103-1110. Armstrong RA (2009j) Spatial correlations between the vacuolation, prion protein (PrPsc) deposits and the cerebral blood vessels in sporadic Creutzfeldt-Jakob disease. Curr Neurovasc Res 6: 239-245. Armstrong RA, Cairns NJ (2009k) Size frequency distribution of the β -amyloid (A β) deposits in dementia with Lewy bodies with associated Alzheimer‘s disease pathology. Neurol Sci 30: 471-477. Armstrong RA, Smith SN (2009l) Carbohydrates in the hypothallus and areolae of the crustose lichen Rhizocarpon geographicum (L.) DC. Symbiosis 49: 95-100. Armstrong RA (2009m) Alzheimer‘s disease and the eye. J Optom 2: 103-111 Hurrell E, Kucerova E, Loughlin M, Caubilla-Barron J, Hilton A, Armstrong RA, Smith C, Grant J, Shoo S, Forsythe S (2009n) Neonatal enteral feeding tubes as loci for colonization by members of the Enterobacteriaceae. BMC Infectious Diseases 9: 146-155. Armstrong RA (2009o) The molecular biology of senile plaques and neurofibrillary tangles in Alzheimer‘s disease. Folia Neuropathol 47: 289-299. Armstrong RA (2010a) A quantitative study of the pathological changes in the cortical white matter in variant Creutzfeldt-Jakob disease (vCJD). In:Handbook on White Matter. Ed: TB Westland, RN Calton, Nova Science Publishers, pp 133-146. Armstrong RA (2010b) The spatial patterns of tau immunopositive neuronal cytoplasmic inclusions (NCI) in the tauopathies. In:Neuroscience Research Advances. Ed: B. Figueredo, F Melandez, Nova Science Publishers, pp 175-189. Armstrong RA, Ellis W, Hamilton RL, Mackenzie IRA, Hedreen J, Gearing M, montine T, Vonsattel JP, Nead E, Lieberman AP, Cairns NJ (2010c) Neuroapthological heterogeneity in frontotemporal lobar degeneration with TDP-43 proteinopathy: a quantitative study of 94 cases using principal components analysis. J Neural Transm 117: 227-239. Armstrong RA, Bradwell T (2010d) Growth of crustose lichens: a review. Geogr Ann 92A: 317. Armstrong RA, Bradwell T (2010e) The use of lichen growth rings in lichenometry: Some preliminary findings. Geogr Ann 92A: 141-147.

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Armstrong RA, Cairns NJ (2010f) Analysis of -amyloid (A) deposition in the temporal lobe in Alzheimer‘s disease using Fourier (spectral) analysis. Neuropathol Appl Neurobiol 36: 248-257. Armstrong RA (2010g) A spatial pattern analysis of -amyloid (A) deposition in the temporal lobe in Alzheimer‘s disease. Folia Neuropathol 48: 67-74. Armstrong RA (2010h) Dispersion of prion protein deposits around blood vessels in variant Creutzfeldt-Jakob disease. Folia Neuropathol 48: 166-174. Armstrong RA (2010i) Lobe formation and division in the foliose lichen Xanthoparmelia conspersa. Symbiosis 51: 227-232. Armstrong RA (2010j) A quantitative study of the pathological changes in the cortical white matter in variant Creutzfeldt-Jakob diseases (vCJD). Clin Neuropathol 29: 390-396. Smith SN, Khan JA, Armstrong RA, Mohindru B, Prince M, Whipps JM (2010k) Acanthamoeba polyphaga trophozoite binding of representative fungal single cell forms. Acta Protozoologica 49: 289-300. Armstrong RA (2010l) Quantitative methods in neuropathology. Folia Neuropathol 48: 217230. Armstrong RA, Cairns NJ (2011a) A morphometric study of the spatial patterns of the TDP43-immunoreactive neuronal inclusions in frontotemporal lobar degeneration with progranulin (GRN) mutation. Histol Histopathol 26: 185-190. Armstrong RA (2011b) Laminar distribution of the pathological changes in sporadic and variant Creutzfeldt-Jakob disease. Pathology Research International. Volume 2011, Article ID 236346, 7 pages. Armstrong RA, Gearing M, Bigio EH, Cruz-Sanchez FF, Duyckaerts, Mckenzie IRA, Perry RH, Skullerud K, Yokoo H, Cairns NJ (2011c) The spectrum and severity of FUSimmunoreactive inclusions in the frontal and temporal lobes of ten cases of neuronal intermediate filament inclusion disease. Acta Neuropathol 121: 219-228. Armstrong RA (2011d) The pathogenesis of Alzheimer‘s disease: A reevaluation of the ―Amyloid Cascade Hypothesis‖. Int J Alz Dis., Vol 2011, Article ID 630865.6 pages. Armstrong RA, Davies L, Dunne MCM, Gilmartin B (2011e) Statistical guidelines for clinical studies of human vision. Ophthal Phys Opt 31: 123-136. Armstrong RA (2011f) Visual signs and symptoms of progressive supranuclear palsy. Clin Exp Optom 94: 150-160. Armstrong RA (2011g) The Spatial Patterns Of -Amyloid (A) Deposits And Neurofibrillary Tangles (NFT) In Late-Onset Sporadic Alzheimer's Disease. In:Alzheimer’s disease: Diagnosis and Treatment, Ed. MR Boyd, Nova Science Publishers, pp 71-82.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 3

BIOGRAPHICAL SKETCH Haruhiko Banno Title: M.D., Ph.D.

Date of Birth: January 17th, 1973

EDUCATION

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Institution and Location Medicine

Degree

Year Conferred

Scientific Field

Contact points [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE Clinical neurology

Professional Appointments Assistant professor

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Publications during last three years

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Banno H, Katsuno M, Suzuki K, et al. Phase 2 trial of leuprorelin in patients with spinal and bulbar muscular atrophy. Ann Neurol. 65: 140-150, 2009. Banno H, Katsuno M, Suzuki K, et al. Neuropathology and therapeutic intervention in spinal and bulbar muscular atrophy. Int J Mol Sci. 10: 1000-1012, 2009.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 4

BIOGRAPHICAL SKETCH Alfred Bennun Title: Bs.As., Arg.

Date of Birth: 07/09/1934

RESEARCH AND PROFESSIONAL EXPERIENCE

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Residences: -to 1962 Arg.; from 10/63 to 10/64, Rehoboth, Israel; from 1965 to 2009, U.S.; 1972, citizen; S.S: #033-30-4179, at present sharing residences in U.S. and Arg. Graduate: 1954: Pharm., School of Medicine, Universidad de Córdoba (U.C.); 1957: M.S. Biochemist, U.C.; 1963: Ph.D. Dr. in Pharm. and Biochm. U.C., Dissertation: 10, summa cum laude. Professional 3/56-/57: 8/57-5/59 honor fellowship by U.C. at Lab. Assoc. Clin. Pathol.; 7/57-1/58: Beth Israel Hospital, Boston and U.C.; 10/58-3/62: Inst. and Rsrch. fellow, Lab. for Cell Metabolism, Nat. Atomic Energy Commission, Arg.; 1962-1963: Rsrch. Invest. full time 3/63-10/63, Dept. of Biol. Chem., School of Medicine, Univ. of B.A.; 1964-1965: Rsrch Associate, Dept. of Physiol. and Pharm., Duke, Durham, N.C.; 1967-1968: Lecturer and 1968-1969: Assist. Prof., Dept. of Biol., University of Puerto Rico; 1969- 1981: Assoc. Prof. of Biochm., Dept. of Zool. and Physiology, NCAS, Rutgers, The State University of N.J., July 1, 1972 tenure; 7/1981-2002 (*): Full Prof. of Biochm., Dept. of Biol. Sci., NCAS, Rutgers (*After retirement research: self-supported).

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Post-doctoral fellowships: 1961-1963: CONICET at School Medicine, U.B.A.; 10/6310/64: • •

at Weizmann Inst. of Sci., Rehovoth, Israel; 1965-1966: 3rd year Postdoctoral, N.I.H., at Pub. Health Research Inst. N.Y.C., Inc.

Major awards 1958: U.S. State Dept. Advance Study Program: Use of radioisotopes in Biol.; 19661967: Special Fellow, NIH, at Dept. Biochemistry, Cornell, Ithaca; 1972: N.A.T.O. Advanced Study Inst. on Primary Molecular Events in Photobiology, Fiesole, Italy. 1 of the 10 plenary lecturers at 3 Symposia of International Union of Biochemistry: 3/12/1975 at 7st Symposium, Berlin; 11/1975 at 75th Symposium, Bogota; and in Arg. Memberships: 1970-1973: Rutgers Scientific Council; Editorial boards: 6 scientific journals; 1970-2002: Full Member Graduate Program in the Molecular Biosciences, Rutgers; Major Thesis Advisor: graduated 8 Ph.D. and 3 M.Sc.;

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Societies: 1970 to present N.Y.A.S., Emeritus 2006.; Discontinued (*): 1969-1982: Am. Chem. Soc., Div. of Biol. Chem.; 1969: Am. Soc. of Plant Physiol.; 1969-1981: Genetics Soc. of Am.; 1969-1974: Am. Nuclear Soc., 1970: Biophys. Soc., Bioenergetics Group; 1972-1974: Fed. Am. Scientists.; 1972- 1981: S.A.I.R. and P.A.A.B.S.; 1974-1978: Am. Soc. for Photobiology. 1974: The Biochemical Soc. (London) and F.E.B.S.; 1977: Am. Soc. of Biol. Chemists, Inc. and F.A.S.E.B.

Publications Bennun, A.; ―Characterization of the norepinephrine-activation of adenylate cyclase suggests a role in memory affirmation pathways. Overexposure to epinephrine inactivates adenylate cyclase, a causal pathway for stress-pathologies‖, Biosystems; 100(2):87-93 (2010) Bennun A. in PubMed: with PhD candidates: Ohanian H, Borhanian K, de Farias S, Bennun A.; ―A model for the regulation of brain adenylate cyclase by ionic equilibria‖, J. Bioenerg. Biomembr., 13(5-6):317-55 (1981). Ohanian H, Borhanian K, Bennun A. ―The effect of manganese on the regulation of brain adenylate cyclase by magnesium and adenosine triphosphate‖, Biochem. Soc. Trans., 6(6):1179-82 (1978); Brydon-Golz S, Ohanian H. & Bennun A.; ―Effects of noradrenaline on the activation and the stability of brain adenylate cyclase‖, Biochem. J., 166(3):473-83 (1977); Brydon-Golz S. & Bennun A.; ―Postsynthetic stabilized modification of adenylate cyclase by metabolites‖, Biochem. Soc. Trans., 3(5):721-4 (1975);

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Research Biographies - Alfred Bennun

15

Vicario PP: ―Separate effects of Mg2+, MgATP, and ATP4- on the kinetic mechanism for insulin receptor tyrosine kinase‖, Biochem Biophys, 278(1):99-105 (1990). ―Role of divalent metals in the kinetic mechanism of insulin receptor tyrosine kinase‖, Arch Biochem Biophys, 261(2):336-45 (1988). Vicario PP, Saperstein R.; ―Role of divalent metals in the activation and regulation of insulin receptor tyrosine kinase‖, Biosystems., 22(1):55-66 (1988). With DeBari V.A.: ―Stimulation of the hexose monophosphate pathway in the human erythrocyte by Mn2+: evidence for a Mn2+-dependent NADPH peroxidase activity‖, Biochem Med., 33(1):1721 (1985). ―Cyclic nucleotide metabolism in the human erythrocyte‖, Clin Physiol Biochem., 2(5):22738 (1984) DeBari VA; ―Cyclic GMP in the human erythrocyte. Intracellular levels and transport in normal subjects and chronic hemodialysis patients‖, Clin Biochem. 15(4):219-21 (1982). With Casciano C.: ―Effect of Li+ on the secretion of HCO3- in rat fundic tissue‖, Biochem Soc Trans., 17(6):1111-2 (1989). ―Investigations on the cytoprotective mechanisms of thiocyanate in rat gastric mucosa‖, Biochem Soc Trans., 17(6):1113-4 (1989) With Harris RH, Cruz R: ―The effect of hormones on metal and metal-ATP interactions with fat cell adenylate cyclase‖, Biosystems., 11(1):29-46 (1979). With Harris R.; ―Hormonal control of fat cells adenylate cyclase‖, Mol Cell Biochem., 10;13(3):141-6 (1976) Energy transduction (titles not included): 10 papers and in 4 books. Bennun A. in Nature New Biology, Vol. 233, 5-8 (1971), showed that R-groups in the electron-carriers transfer excitation-energy by the dipole state dynamics of metal-coordinative-chemistry of carriers in (turnover of electron-entanglement). Resolution and reconstitution of enzymemembrane systems, with Avron M., reported in Biochimica et Biophysica acta 109, 117127 (1965), and with Racker E. The Journal of Biological Chemistry, 244, 1325-1331 (1969). Bennun A. describes the shape-change of actin by ATP binding dynamics, ―In Mechanism of energy transduction in biological system‖, (Green D.E., ed.), Annals New York Academy of Sciences, 227, 116-145 (1974). Bennun A. describes the open system lungs-blood, in which the mass-action of pO2 and ÄpH induces free energy-dependent changes. The molecular description shows metabolite control feedback of Hb by a mutually exclusive control of the reactivity of Hb R-groups in Biomed. Biochim. Acta. 46, No 23, 314-319 (1987).

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Abram A. Chernyovskaya and Graviil F. Klossovsky

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 5

BIOGRAPHICAL SKETCH Kim M. Cecil Title: PhD Professor of Radiology, Pediatrics, Neuroscience and Environmental Health, Cincinnati Children‘s Hospital Medical Center (CCHMC) and the University of Cincinnati College of Medicine

Date of Birth: 1967

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EDUCATION Institution and Location Vanderbilt University, Postdoctoral Fellowship at the Hospital of the University of Pennsylvania

Degree

Year Conferred

Scientific Field

BS, MS, PhD

Contact points Address: 3333 Burnet Avenue, MLC 5033, Cincinnati, OH 45229

RESEARCH AND PROFESSIONAL EXPERIENCE Spectroscopist at CCHMC since 1998, Assistant Professor 2000-2004, Associate Professor 2004-2008, Professor 2008 to present

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Professional Appointments Cincinnati Children‘s Hospital and the University of Cincinnati College of Medicine Honors 2000- Derek Harwood Nash Award for Research in Pediatric Neuroradiology, American Society of Neuroradiology; 2003- Point of Care Award, American Association for Clinical Chemistry; 2008-Caffey Award for the Best Clinical Science or Education Paper, Society for Pediatric Radiology; 2008- General Neuroradiology Outstanding Presentation Award, American Society of Neuroradiology

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Publications during last three years 1. ―Late Proton MR Spectroscopy Following Traumatic Brain Injury During Early Childhood: Relationship with Neurobehavioral Outcomes,‖ Nicolay C. Walz, Kim M. Cecil, Shari L. Wade and Linda Michaud, Journal of Neurotrauma 2008, 25, 94-103. 2. ―Temporal Change in N-acetyl-Aspartate Concentrations in Adolescents with Bipolar Depression Treated with Lithium,‖ Nick C. Patel, Melissa P. DelBello, Kim M. Cecil, Caleb M. Adler, Kevin E. Stanford, and Stephen M. Strakowski, Journal of Child and Adolescent Psychopharmacology 2008, 18, 132-139. 3. ―Decreased Brain Volume in Adults with Childhood Lead Exposure,‖ Kim M. Cecil, Christopher J. Brubaker, Caleb M. Adler, Kim N. Dietrich, Mekibib Altaye, John C. Egelhoff, Stephanie Wessel, Ilayaraja Elangovan, Kelly Jarvis and Bruce P. Lanphear, PLoS Medicine 2008, 5(5), 741-750 (e112 doi:10.1371/journal.pmed.0050112). 4. ―Neurochemical Alterations in Adolescent Bipolar Depression: A Proton Magnetic Resonance Spectroscopy Pilot Study of the Prefrontal Cortex,‖ Nick C. Patel, Kim M. Cecil, Stephen M. Strakowski Caleb M. Adler, and Melissa P. DelBello, Journal of Child and Adolescent Psychopharmacology 2008, 18, 623-627. 5. ―Megalencephalic Leukoencephalopathy with Subcortical Cysts (MLC): a third confirmed case with literature review,‖ Lili Miles, Ton J. deGrauw, Argirios Dinopoulos, Kim M. Cecil, Marjo S. van der Knaap, and Kevin E. Bove, Pediatric and Developmental Pathology 2009, 12, 180-186. 6. ―Altered Myelination and Axonal Integrity in Adults with Childhood Lead Exposure: A Diffusion Tensor Imaging Study,‖ Christopher J. Brubaker, Vincent J. Schmithorst, Erin N. Haynes, Kim N. Dietrich, John C. Egelhoff, Diana M. Lindquist, Bruce P. Lanphear, and Kim M. Cecil, Neurotoxicology 2009, 30, 867-875. 7. ―Correlation of Diffusion Tensor Imaging with Executive Function Measures After Early Childhood Traumatic Brain Injury,‖ Brad Kurowski, Shari L. Wade, Kim M. Cecil, Nicolay C. Walz, Weihong Yuan, Akila Rajagopal and Scott K. Holland, Journal of Pediatric Rehabilitation Medicine: An Interdisciplinary Approach 2010, 2, 273-283.

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Research Biographies - Kim M. Cecil

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8. ―The Influence of Age of Lead Exposure on Adult Gray Matter Volume,‖ Christopher J. Brubaker, Kim N. Dietrich, Bruce P. Lanphear, and Kim M. Cecil, Neurotoxicology 2010, 31, 259-266. 9. ―Effects of Early Low-Level Lead Exposure on Human Brain Structure, Organization and Functions,‖ Kim M. Cecil, Journal of Developmental Origins of Health and Disease, 2011, 2, 17-24. 10. ―Proton Magnetic Resonance Spectroscopy in Adults with Childhood Lead Exposure,‖ Kim M. Cecil, Kim N. Dietrich, Mekibib Altaye, John C. Egelhoff, Diana M. Lindquist, Christopher J. Brubaker, and Bruce P. Lanphear, Environmental Health Perspectives 2011, 119, 403-408. 11. ―Long Term Antipsychotic Treatment Does Not Alter Metabolite Concentrations in Rat Striatum: An In Vivo Magnetic Resonance Spectroscopy Study, Diana M. Lindquist, R. Scott Dunn and Kim M. Cecil, Schizophrenia Research 2011, Mar 21 e-publication.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 6

BIOGRAPHICAL SKETCH Malka Cohen-Armon Title: D.Sc. Tel-Aviv University, Sackler School of Medicine

Date of Birth: Aug. 7 1949

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EDUCATION Institution and Location Chemist IIT, Technion, Israel Institute of Technology

Degree

Year Conferred

Scientific Field

Contact points Address: Sackler School of Medicine, Dept. Physiology and Pharmacology, Cardiac Research Institute. PO Box 39040, 69978 Tel-Aviv, Israel.

Academic Background 1969-1972 Technion-IIT Israel, B.Sc. (Cum Laude), Chemistry 1973-1974 Technion-IIT Israel, M.Sc., A molecular mechanism underlying the voltage dependent Na channel function. Supervised by Prof. Yoram Palti, Physiology and Biophysics 1974-1980 Technion-IIT Israel, D.Sc. Experimental examination of the molecular model underlying the voltage dependent Na channel function. Superviser Prof. Yoram Palti Physiology and Biophysics

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Previous Employment 1977-1981 Technion-IIT, Israel, Lecturer/Instructor, Electrophysiology and Biophysics 1983-1991 Tel-Aviv University, post-doc position. Training in Neurobiochemistry in the lab of Prof. Mordechai Sokolovsky) Faculty of Life Sciences Tel-Aviv University, Faculty 1992-2011 Faculty in Sackler School of Medicine, Dept of Physiology & Pharmacology and the Neufeld Cardiac Research Institute 2001- Visiting professor in Columbia University, NY, Center for Neurobiology and Behavior. Lab of Prof. James H. Schwartz. HFSP fellowship to Dr. Cohen-Armon. 2007- Associate Professor, Sackler School of Medicine, Dept of Physiology & Pharmacology and the Neufeld Cardiac Research Institute

Research topics Signal transduction mechanisms, Neurobiology, biochemical mechanisms of memory formation, Epigenetic mechanisms, PARPs and polyADP-ribosylation, Mechanism of cancer therapy.

Member of the Editorial board of

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Am. J. of Alzheimer's Disease & Other Dementias Member of Editorial Board of Signal Transduction Insights Prizes, grant and donations 2006-2011 2010-2011 NIH grant 1R21DA027776. Treatment of cocaine craving and relapse by memory erasure, in collaboration with Prof. Yadid, Bar –Ilan University, 200,000 $ Feingrout Foundation-Medicine Faculty, Breast Cancer Therapy, 10000 $ 2006-2009- ISF- The involvement of PARPs in biological clocks. In collaboration with Dr. Moran, Hebrew University 199,000 $ 2006-2009 Israel Ministry of Health PolyADP-ribosylation regulate expression of genes associated with long-term memory 35000 $, 2004-2007 ISF: PARP-1 is activated by ERK2: What is the mechanism? 100,000 $ The National Institute for Psychobiology: PolyA P-ribosylation of chromatin-bound proteins and memory formation Neuronal signaling to the nuclear protein PARP-1. 150,000 $

Relevant selected papers Homburg, S., Visochek, L., Moran, N., Dantzer, F., Priel, E., Asculai, E., Schwartz, D., Rotter, V., Dekel, N., and Cohen-Armon, M. (2000) A fast signal-induced activation of poly(ADP-ribose) polymerase: A novel downstream target of phospholipase C. J. Cell Biol. 150 (2):293-307. Editorial: ‗Depolarization activates PARP‘ 150 (2):2.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Cohen-Armon M., Visochek L., Katzoff A., Levitan D., Susswein A.J., Klein R., Valbrun M., and Schwartz J.H. (2004) Long-term memory requires polyADP-ribosylation. Science 304: 1820-1823. Editorial: ‗DNA damage and Long-Term Memory‗, 1715. Visochek L., Steingart R., Vulih R.A., Klein R., Priel E., Gozes I., and Cohen-Armon M. (2005) PolyADP-ribosylation is involved in neurotrophic activity. J. Neurosci. 25:7420-7428. Editorial: PARP-1 activation and neurotrophins. Cohen-Armon M., Visochek L., Priel E., and Ishai J. S. 2006. PARP mediated fatal effect of hornet venom in rat brain cortical neurons. Chemistry & Biodiversity 3:535-43 Cohen-Armon M., Visochek L., Rozensal D., Kalal A., Klein R., Bendetz- Netzer S., Yao Z., and Seger R. (2007) DNA-independent PARP-1 activation by phosphorylated ERK2 increases Elk1 activity: A link to histone acetylation. Mol. Cell 25: 297-308 Cohen-Armon M. (2007) PARP-1 activation in the ERK signaling pathway Trend Pharmacol. Sci. 28: 556-560 Goldberg S., Visochek L, Giladi E., Gozes I., and Cohen-Armon M. (2009) PolyADPribosylation is required for long-term memory formation in mammals. J. Neurochem. 111:72-79. Kalal Adi, Visochek Leonid, Cohen-Armon Malka (2011) PARP-1-ERK interaction is required for immediate early genes expression in response to electrical stimulation in cerebral neurons (under revision)

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Last 3 years papers Goldberg S., Visochek L, Giladi E., Gozes I., and Cohen-Armon M. (2009) PolyADPribosylation is required for long-term memory formation in mammals. J. Neurochem. 111:72-79. Inbar-Rozensal D., Visochek L., Castel D., Castiel A., Izraeli S., Dantzer F. and CohenArmon M. (2009) A selective eradication of human nonhereditary breast cancer cells by phenanthridine -derived polyADP-ribose polymerase inhibitors. Breast Cancer Res. 11(6):R78. Editorial: Kristine M Frizzell, W Lee Kraus (2009) PARP inhibitors and the treatment of breast cancer: beyond BRCA1/2? Breast Cancer Research, 11:111 Press release: http://www.eurekalert.org/pub_releases/2009-11/bc-sot110309. php Geistrikh I., Visochek L., Klein R., Miller L., Shainberg A. and Cohen-Armon M. (2011) Ca2+ induced PARP-1 activation and ANF expression are coupled events in cardiomyocytes Biochem J. 2011 Jun 2. [Epub ahead of print] Asher Castiel, Leonid Visochek, Shai Izraeli, Françoise Dantzer, Malka Cohen-Armon (2011) A small molecule exclusively eradicates human cancer cells: Extra-centrosomes declustering agent (under revision) Kalal Adi, Visochek Leonid, Cohen-Armon Malka (2011) PARP-1-ERK interaction is required for immediate early genes expression in response to electrical stimulation in cerebral neurons (under revision)

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 7

BIOGRAPHICAL SKETCH Paola De Bartolo Title: 1. Department of Psychology, ―Sapienza‖ University of Rome, Rome, Italy; 2. I.R.C.C.S. Fondazione S. Lucia, Rome, Italy.

Date of Birth: November, 30, 1979

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EDUCATION Institution and Location PhD awarded 12/12/2007

Degree

Year Conferred

Scientific Field

Contact points Address: via dei Marsi, 78 00185 Rome, Italy; mail: [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE Dr. De Bartolo carries out her research activity since 2001 at the Laboratory of Experimental and Behavioural Neurophysiology, directed by Prof. Petrosini, in the IRCCS S. Lucia in Rome. Her activity is addressed to two main research fields, investigated by means of neuroanatomical and behavioural methods. The first one concerns the study of cerebellar functions and structures and their relations with other subcortical and cortical areas, by using a rat model of hemicerebellectomy. In particular, the most recent investigations have been focused on the cortico-striatal circuits and the local expression of Calcium-Binding Proteins.

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Abram A. Chernyovskaya and Graviil F. Klossovsky

The second research field concerns the study of CNS morphological and functional changes in a rat model of Alzheimer‘s disease, such as cholinergic depletion of basal forebrain. Depletion effects are also evaluated in the presence of pharmacological and experiential factors. More specifically, dendritic branching and spine density in pyramidal neurons, neuronal metabolic activity and spatial functions were analysed. Furthermore, in last period an animal model of deafness is object of her research. In particular she is analysing cerebral structural changes following periferical damage and the eventual neuroprotective effect of an antioxidant drug. The results of this study have been object of several presentations at international meetings and works submitted to prestigious international journals.

Professional Appointments Associate Researcher

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Publications during last three years (2009-2011) 1. De Bartolo P, Gelfo F, Burello L, De Giorgio A, Petrosini L, Granato A. Plastic Changes in Striatal Fast-Spiking Interneurons Following Hemicerebellectomy and Environmental Enrichment. Cerebellum. 2011 Apr 21. [Epub ahead of print] PubMed PMID: 21509479. IF: 3.3. 2. Gelfo F, De Bartolo P, Tirassa P, Croce N, Caltagirone C, Petrosini L, Angelucci F. Intraperitoneal injection of neuropeptide Y (NPY) alters neurotrophin rat hypothalamic levels: implications for NPY potential role in stress-related disorders. Peptides. 2011 Apr 4. [Epub ahead of print] PubMed PMID: 21473895. IF: 2.7. 3. Gelfo F, Tirassa P, De Bartolo P, Caltagirone C, Petrosini L, Angelucci F. Brain and Serum Levels of Nerve Growth Factor in a Rat Model of Alzheimer's Disease. J Alzheimers Dis. 2011 Mar 2. [Epub ahead of print] PubMed PMID: 21368378. IF: 5.1 4. Cutuli D, Rossi S, Burello L, Laricchiuta D, De Chiara V, Foti F, De Bartolo P, Musella A, Gelfo F, Centonze D, Petrosini L. Before or after does it matter? Different protocols of environmental enrichment differently influence motor, synaptic and structural deficits of cerebellar origin. Neurobiol Dis. 2011 Apr;42(1):9-20. Epub 2010 Dec 21. PubMed PMID: 21182946. IF: 4.5. 5. Foti F, Laricchiuta D, Cutuli D, De Bartolo P, Gelfo F, Angelucci F, Petrosini L. Exposure to an enriched environment accelerates recovery from cerebellar lesion. Cerebellum. 2011 Mar;10(1):104-19. PubMed PMID: 21113697. IF: 3.3. 6. Gelfo F, Cutuli D, Foti F, Laricchiuta D, De Bartolo P, Caltagirone C, Petrosini L, Angelucci F. Enriched environment improves motor function and increases neurotrophins in hemicerebellar lesioned rats. Neurorehabil Neural Repair. 2011 Mar-Apr;25(3):24352. Epub 2010 Oct 21. PubMed PMID: 20966156. IF: 5.4.

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7. De Bartolo P, Cutuli D, Ricceri L, Gelfo F, Foti F, Laricchiuta D, Scattoni ML, Calamandrei G, Petrosini L. Does age matter? Behavioral and neuro-anatomical effects of neonatal and adult basal forebrain cholinergic lesions. J Alzheimers Dis. 2010 Apr;20(1):207-27. PubMed PMID: 20164586. IF: 5.1. 8. Foti F, Mandolesi L, Cutuli D, Laricchiuta D, De Bartolo P, Gelfo F, Petrosini L. Cerebellar damage loosens the strategic use of the spatial structure of the search space. Cerebellum. 2010 Mar;9(1):29-41. PubMed PMID: 19798544. IF: 3.3. 9. Mandolesi L, Foti F, Cutuli D, Laricchiuta D, Gelfo F, De Bartolo P, Petrosini L. Features of sequential learning in hemicerebellectomized rats. J Neurosci Res. 2010 Feb 15;88(3):478-86. PubMed PMID: 19746422. IF: 3.0. 10. Angelucci F, De Bartolo P, Gelfo F, Foti F, Cutuli D, Bossù P, Caltagirone C, Petrosini L. Increased concentrations of nerve growth factor and brain-derived neurotrophic factor in the rat cerebellum after exposure to environmental enrichment. Cerebellum. 2009 Dec;8(4):499-506. Epub 2009 Aug 19. PubMed PMID: 19688409. IF: 3.3. 11. Petrosini L, De Bartolo P, Foti F, Gelfo F, Cutuli D, Leggio MG, Mandolesi L. On whether the environmental enrichment may provide cognitive and brain reserves. Brain Res Rev. 2009 Oct;61(2):221-39. Epub 2009 Jul 23. Review. PubMed PMID: 19631687. IF: 7.4. 12. De Bartolo P, Gelfo F, Mandolesi L, Foti F, Cutuli D, Petrosini L. Effects of chronic donepezil treatment and cholinergic deafferentation on parietal pyramidal neuron morphology. J Alzheimers Dis. 2009 May;17(1):177-91. PubMed PMID: 19494441. IF: 5.1. 13. De Bartolo P, Mandolesi L, Federico F, Foti F, Cutuli D, Gelfo F, Petrosini L. Cerebellar involvement in cognitive flexibility. Neurobiol Learn Mem. 2009 Oct;92(3):310-7. Epub 2009 Apr 9. PubMed PMID: 19362159. IF: 3.5. 14. Gelfo F, De Bartolo P, Giovine A, Petrosini L, Leggio MG. Layer and regional effects of environmental enrichment on the pyramidal neuron morphology of the rat. Neurobiol Learn Mem. 2009 May;91(4):353-65. PubMed PMID: 19340947. IF: 3.5. 15. Cutuli D, Foti F, Mandolesi L, De Bartolo P, Gelfo F, Federico F, Petrosini L. Cognitive performances of cholinergically depleted rats following chronic donepezil administration. J Alzheimers Dis. 2009 May;17(1):161-76. PubMed PMID: 19221411. IF: 5.1.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 8

BIOGRAPHICAL SKETCH Valentina Echeverria Title: Scientist (Bay Pines VA Healthcare System); Assistant Professor (University of South Florida)

Date of Birth:

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EDUCATION Institution and Location University of Concepcion, Chile University of Concepcion, Chile University of Concepcion, Chile National Centre of Biotechnology (CSIC), Spain McGill University, Canada Johns Hopkins University, USA

Degree

Year Conferred

Scientific Field

Biochemist

1984-1989

Biochemistry

M.S.

1991-1994

Biochemistry

Ph.D.

1994-1999

Biological Sciences

Post-Doctoral

1999-2001

Neuroscience

Post-Doctoral

2001-2003

Neuroscience

Post-Doctoral

2003-2005

Neuroscience

RESEARCH AND PROFESSIONAL EXPERIENCE Employment 2009-Present 2007-2009

Scientist, VA Healthcare System, FL, USA; Assistant Professor, University of South Florida, Tampa, USA. Scientist, Bay Pines Foundation, Inc. FL, USA; Assistant Professor, University of South Florida, Tampa, USA

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Abram A. Chernyovskaya and Graviil F. Klossovsky

30 2005-2006

2000-2001 1999 1996-1998 1996

Assoc. Res. Scientist. The Taub Institute for Research on Alzheimer‘s disease and the Aging Brain and Dept. of Pathology, Columbia University, New York City, USA. Research Scientist. National Center of Biotechnology CNB (CSIC), Madrid, Spain Postdoctoral Fellow, Instituto Cajal (CSIC), Madrid, Spain Research Scientist, Biochemistry Department, Faculty of Medicine, Alcala, Madrid, Spain. Research Scientist, Plant Physiology Institute DIFCA, University of Milan, Italy.

Honors • • •

• • •

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Travel Award to present at the International Conference of Alzheimer‘s Disease (ICAD). Alzheimer‘s Association (2008) Young Investigator Educational Enhancement Award. American Society of Neurochemistry (2004) Stage of foreign scientist in Spain. Contract from Science and Technology Ministry of Spain. Molecular and Cellular Biology National Center of Biotechnology (CSIC).Madrid, Spain. (Intl. Competition)(2000, 2001) Teaching assistant Doctoral fellowship. Graduate school. University of Concepción, Chile. (1999) Doctoral fellowship from National Commission of Science and Technology, CONICYT, Chile (1995-1998) Teaching assistant Graduate fellowship. Graduate school. University of Concepción, Chile. (1991-1994) Fellowship to participate in The In Vitro Cell Biology and Biotechnology program (700 hrs study) at M.A.R. Institute, Chazy, NY, The S.U.N.Y. Plattsburgh, NY. USA. (Intl. competition) (1993)

Professional Affiliations Member, New York Academy of Sciences, 2005-Present Member, American Society of Neurochemistry, 2004 Member, American Society of Neurosciences, 2004-Present Honorary Member. The Scientific Research Society Sigma Xi, 1992.

PUBLICATIONS Peer-Reviewed journal publications Zeitlin R, Patel S, Burgess S, Gamble-George J, Arendash GW, Echeverria V, Cell signaling changes induced by caffeine in the striatum of APPswe mice.Submitted, 2010

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Echeverria V, Zeitlin R, Burgess S, Zeitlin R, Barman A, Thakur G, Inouye H, Feris E, Sattelle D, Kirschner DA, Mori T, Leblanc R, Prabhakar R, and Arendash G. Cotinine Reduces Amyloid  Aggregation and Improves Memory in Alzheimer‘s Mice.Under Review, 2010. Burgess S, Echeverria V. Raf Inhibitors as Therapeutic Agents against Neurodegenerative Diseases. CNS. Neurol. Disord. Drug Targets. 9(1):120-7, 2009. Echeverria V, Burgess S, Gamble-George J, Zeitlin RS, Mamcarz M, Cao C, Arendash GW. Sorafenib inhibited cRaf-1/NFB pathway and restored working memory in aged APPswe mice. Neuroscience162, (4):1220-1231, 2009. Arendash GW, Mori T, Mamcarz M, Dickson A, Runfeldt M, Rezai-Zadeh K, Citron B, Tan J, Lin X, Cao Ch, Echeverria V, and Potter H. Caffeine reverses cognitive impairment and decreases brain Aβ levels in aged Alzheimer‘s mice. J. Alzheimer’s Disease 17(3)661-80, 2009. Echeverria V, Burgess S, Gamble-George J, Arendash GW, Citron AB. Raf inhibition is Neuroprotective against Amyloid  toxicity. Neuroscience Letters. Oct 17; 444 (1):92-96, 2008. Citron, B A., Dennis, J S., Zeitlin, RS., Echeverria V. Transcription factor Sp1 dysregulation in Alzheimer‘s Disease. J Neuroscience Res. Aug 15;86(11):2499-504, 2008. Echeverria V, Powell D, Arancio O. Oligomers of -amyloid peptide block BDNF-induced Arc expression in cultured cortical neurons. Current Alzheimer Research. 4 (5):518-52, 2007. Ahmad M, Saalem S, Zhuang H, Echeverria V, Sapirstein A, Doré, S. 1-hydroxyPGE1 reduces infarction volume in mouse transient cerebral Ischemia. European Journal Neuroscience. 23(1):35-42, 2006. Echeverria V, Clerman A., Doré, S. Stimulation of PGE receptors EP2 and EP4 protects cultured neurons against oxidative stress and cell death following beta-amyloid exposure. European Journal Neuroscience. 22(9): 2199-206, 2005. Echeverria V, Ducatenzeiler A, Chen CH, Cuello AC. Endogenous beta- amyloid peptide synthesis modulates cAMP response element-regulated gene expression in PC12 cells. Neuroscience. 135(4): 1193-202, 2005. Echeverria, V, Greenberg LD, Doré, S. Expression of Prostaglandin E2 Synthases in mouse postnatal cortical neurons. Ann NY Acad Sci., 1053:460-71, 2005. Echeverria V, Dowd E., Ducatenzeiler A, Alohen L, Janne J, Grant S, Muro A, Baralle F, Li H, Hartmann, T, Cuello, AC. Altered mitogen-activated protein kinase signaling, tau hyperphosphorylation and mild spatial learning dysfunction in transgenic rats expressing the beta-amyloid peptide intracellularly in hippocampal and cortical neurons. Neuroscience. 129(3): 583, 2004. Echeverria V, Ducatenzeiler A, Alohen L, Janne J, Grant S, Wandosell F, Muro A, Baralle F, Li H, Duff K, Szyf M, Cuello AC. Rat transgenic models with a phenotype of intracellular A accumulation in hippocampus and cortex. J Alzheimer’s Disease. 6(3): 209–19, 2004. Echeverria V, Cuello AC. Intracellular A amyloid, a sign for worse things to come? Mol Neurobiol 26(2-3): 299–316, 2002

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Ledo F, Link W, Carrión A, Echeverría V, Mellstrom B, Naranjo JR. The DREAM-DRE interaction:key nucleotides and dominant negative mutants. Biochemica et Biophysica Acta 14676: 1–7, 2000 Echeverría V, Hinrichs MV, Torrejón M, Ropero S, Toro MJ, Olate J. Mutagenesis in the switch IV of the helical domain of the human Gsreduces its GDP/GTP exchange rate. J Cell Biochem 76(3): 368–375, 1999. Torrejón M, Geneviere A.M, Echeverría V, Guzmán L, Hinrichs M, Olate J. The C2 cytosolic loop of adenylyl cyclase interacts with the activated form of Gs. FEBS Letters. 441: 437–440, 1998. Torrejón M, Echeverría V, Retamales G, Herrera L, Hinrichs M, Olate J. Molecular cloning and expression of an adenylyl cyclase from Xenopus laevis oocytes. FEBS Letter 404: 91–94, 1997. Echeverría V, Olate J, Cid H. Partial DNA Sequence of a -lactamase produced by a Shigella flexneri strain. Microbios. 83: 107–117, 1995. Echeverría V, Mondaca MA, Montoya R, Bunster M, Cid H. Characterization of a plasmid codifying the synthesis of a -lactamase produced by Shigella flexneri. Microbios 76:161–166, 1993. Book Chapters Echeverria V and Zeitlin R. Cotinine: Implications in Neurological and Psychiatric Disorders. In: ―Working Memory: Capacity, Developments and Improvement Techniques‖. NOVA Science Publishers. Accepted. Dec, 2010. Cuello AC, Bell KFS, Echeverria V, Lopez E, Ribeiro-da-Silva A, Szyf, M. The impact of extracellular amyloid- (A) peptides on cortical neurotransmitters and of intracellular A accumulation on protein expression. In Recent progress in Alzheimer‘s and parkinson‘s Diseases. Hanin, I, Cacabelos R and Fisher A Ed. Taylor & Francis London and NY.44: 347-354, 2005 Abstracts (Selected) Echeverria V, Burgess S, Zeitlin R, Barman A, Thakur G, Inouye H, Feris E, Kirschner DA, Mori T, Leblanc RM, Prabhakar R and Arendash GW. Cotinine Reduces Amyloid Burden and Improves Cognitive Abilities in Tg6799 Mice.15th Intl. Conference on Alzheimer‘s Disease and Related Disorders. 2010. Honolulu, HI, USA Gamble-George J, Burgess S., Echeverria V. Cotinine reduces fear-induced anxiety and enhances the extinction of the fear memory 38th. Annual Meeting of the Society for Neuroscience. 2009. Chicago. IL. USA. Gamble-George J, Burgess S, Echeverria V. Chronic Caffeine Treatment Restores Arc Expression and Promotes DARPP-32/PKA Signaling. Conference on Alzheimer‘s Disease and Related Disorders. 2008. Chicago. IL. USA. Gamble-George J, Burgess S, Arendash G, Echeverria V. Caffeine Stimulates Dopamine and Cyclic AMP-Regulated Phosphoprotein and Activity-Regulated Cytoskeleton-Associated Protein. Second Annual Signature Interdisciplinary Program in Allergy, Immunology, and Infectious Disease (SIPAIID) Symposium Immunity and Pathogens. May 9th. 2008.Tampa. FL. USA.

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Burgess S, Zeitlin R, Gamble-George J, Echeverria V. Sorafenib as a therapeutic agent against Alzheimer‘s Disease. 13th Intl. Conference on Alzheimer‘s Disease and Related Disorders. 2008. Chicago. IL. USA. Echeverria V, Gamble-George J, Burgess S, Dickson A, Mamcarz M. 13th Intl. Cotinine as a therapeutic drug against Alzheimer‘s disease. Conference on Alzheimer‘s Disease and Related Disorders. 2008. Chicago. IL. USA. Echeverria V, Dennis JS, Arendash G and Citron BA. cRaf-1 dysregulation in Alzheimer disease: new insights about the molecular therapeutic mechanisms of caffeine. 37th Annual Meeting of the Society for Neuroscience. 3-7 Nov 2007.San Diego. CA. Selected for press release. Echeverria V, D. C. Powell DC, Arancio O. Deficiency in synaptic plasticity in TgAPP/PS1 mice is accompanied by CaMK II dysregulation in hippocampus. 36th Annual Meeting of the Society for Neuroscience. October 2006. Atlanta. GA. Echeverria V, Clerman A., Dore S. Stimulation of PGE2 EP2 and EP4 receptors suppresses βamyloid-induced oxidative stress in mouse cultured postnatal neurons. 35th Annual Meeting of the Society for Neuroscience. November 2005. Washington DC. Ahmad, M., Saleem, S., Zhuang, H., Echeverria, V., Sapirstain, A., Dore, S. D-hydroxyPGE1 reduces infarction volume in mouse transient cerebral ischemia. 35th Annual Meeting of the Society for Neuroscience. November 2005. Washington DC. Doré S, Echeverria V. PGE2 receptors modulate the β -amyloid toxicity in cultures of mouse postnatal neurons. 34th Annual Meeting of the Society for Neuroscience. October 2004. San Diego CA. Echeverria V, Greenberg D, Doré S. Characterization of the protein expression profile of eicosanoid metabolism enzymes and prostanoid receptors in postnatal neuronal cultures. 34th Annual Mtg. of the Society of Neuroscience. Oct. 2004. San Diego CA. Echeverria V, Greenberg D, Doré S. Modulation of β -amyloid neurotoxicity by PGE2 EP prostaglandin receptor agonists in postnatal cultured mouse neurons. Annual Mtg. of the American Society for Neurochemistry. Aug. 2004. NY, NY. Doré S, Zhuang H, Echeverria V, Kim YS. Metabolites of COX pathway can be neuroprotective. Annual Mtg.of the American Society for Neurochemistry. Aug. 2004. New York NY. Cuello AC, Ducatenzeiler A, Echeverria V. Possible Pathological and Physiological Roles for Intracellular Aβ peptides. 9th Intl. Conference on Alzheimer‘s Disease and Related Disorders. July 2004. Philadelphia PA. Echeverria V, Doré S. β -amyloid neurotoxicity is modulated by PGE2 actions: specific role of EP1 to EP4 receptors. 9th Intl. Conference on Alzheimer‘s Disease and Related Disorders. July 2004. Philadelphia PA. Echeverria V, Ducantenzeiler A, Cuello AC. A physiological role for Aβ fragments? 33rd Annual Mtg. of the Society for Neuroscience, Nov. 2003, New Orleans LA. Cuello AC, Echeverria V, Bell KFS, Lopez E, Ribeiro-da-Silva A, Szyf M. The impact of extracellular Aβ peptides on cortical neurotransmitters and of intracellular accumulation th

on protein expression. 6 Intl. Conf. AD/PD, May 2003, Sevilla, Spain.

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Echeverria V, Dowd E, Alhonen L, Janne J, Duff K, Ducantenzeiler A, Grant S, Muro A, Baralle F, Szyf M, Wandossel F, Avila J, Cuello AC. A rat transgenic model over expressing intraneuronal human A β peptide shows tau hyperphosphorylation and MAPK activation. 32nd Annual Mtg. of the Society for Neuroscience, Nov. 2002. Slide Presentation 522.3. Cuello AC, Echeverria V, Dowd E, Lopez E, Vercauteren F, Bell K, Ribeiro-da-Silva A, Szyf, M. The impact of Intracellular Aβ peptides. The 11th Annual Meeting of the Israel Society for Neuroscience, Dec. 2002, Eilat, Israel. Echeverria V, Dowd E, Alhonen L, Janne J, Duff K, Ducantenzeiler A, Grant S, Muro A, Baralle F, Szyf M, Wandossel F, Avila J, Cuello AC. A rat transgenic model expressing human amyloidgenic A β peptide intraneuronally in the hippocampus and cortex shows up-regulation of activated MAPK and tau hyperphosphorylation. Alzheimer Ass. Mtg., 2002, Stockholm, Sweden. Echeverria V. Protein-protein interactions of transcriptional repressor DREAM. 23rd Annual Meeting of The Neurochemistry Association. Biochemistry and Molecular Biology Annual Mtg., 2000, Granada, Spain. Olate J, Torrejon M, Hinrichs MV, Echeverria V. Mutagenesis in the switch IV region of the helical domain of the human Gs affects its guanine nucleotide binding capacity. 39th Annual Mtg. of the American Society for Cell Biology (ASCB). Dec. 1999, Washington, DC. Hinrichs MV, Echeverría V, Torrejón M, Toro MJ, Olate J. Mutagenesis in the Switch IV region of the helical domain of the human Gs reduces its guanine nucleotide interchange rate. 42nd Ann. Mtg. Biology Society of Chile, 1999, Chile. Echeverría V, Toro MJ, Olate J. Functional properties of the helical domain of the Gs subunit. 26th Annual Mtg. of the Federation of European Biochemical Societies. June 1924, 1999. Olate J, Echeverría V, Guzmán L, Hinrichs MV, Geneviére A-M, Torrejón M. Adenylyl cyclase regulation by the Gs protein: a molecular analysis. 21st Annual Mtg. of the Biochemistry and Molecular Biology Society, 1999, Valdivia, Chile. Echeverría V, Hueltes MC, Olate J, Toro MJ. A possible role of Gs helical domain in β adrenergic receptor coupling. 4th European Endocrinology Congress, Sevilla, Spain, May, 1999.

EDITORIAL BOARDS Neural Regeneration Research-2010 American Journal of Alzheimer’s disease and Other Dementias. 2005 Ad Hoc reviewer Neuroscience 2006-Present J Neurotrauma 2007-Present BMC-Neuroscience 2008-Present Neurotox. Research 2008-Present J Neuroinmunology 2008-Present Experimental Neurology 2009-Present

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Neuroscience Letters 2009-Present Expert Opinion 2010-Present On Investigational Drugs Neural Regeneration 2010-Present Research Others Reviewer-Alzheimer’s Association

GRANTS

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Ongoing  2010-2013 Echeverria V (PI) $583,000 James and Esther King Florida Biomedical Research Program, Florida, 95 % effort. Subject: Investigating Cotinine to Improve Memory and Prevent Tobacco Abuse in Subjects with Cognitive Impairment due to Psychiatric Disorders.  2008-2010 Echeverria V (PI) $100,000 Alzheimer‘s Association. New Investigator Grant, 10% effort Molecular Mechanisms Underlying the neuroprotective actions of Cotinine. Completed  2007-2010 Echeverria V (PI) $375,000 James and Esther King Florida Biomedical Research program New Investigator Award, Florida, 75 % effort. Subject: Tobacco-research, Effect of cotinine in the CNS.  2008 Echeverria V (PI) $50,000 Grant Johnnie B. Byrd Sr. Alzheimer‘s Center and Research Institute,Tampa, Florida, 5% effort, 1 year. Pilot grant. Cotinine as a Therapeutic agent against AD.  2007 Echeverria V (PI) $50,000 Grant Johnnie B. Byrd Sr. Institute of Alzheimer‘s Center and Research Institute, Florida,, 10% effort, 1 year. Pilot grant. Cell signalling factors in Alzheimer‘s disease. Subject: Study of Sp1 and Raf inhibition in Alzheimer‘s Disease Pathology.  1997–1998 Echeverria V (PI) $20,000 Grant Award FONDECYT #2970061. Chile. ―Functional characterization of Gs helical domain from G protein‖ (Competition opened to PhD Students).

Submitted NIH R01 Echeverria V (PI) Jun5, 2010, $1,489,788 ―Characterizing the Molecular Mechanisms Underlying the Beneficial Effects of Cotinine against Alzheimer‘s Disease‖.

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Abram A. Chernyovskaya and Graviil F. Klossovsky

36 PATENTS Provisional

1. The use of cotinine as a therapeutic Agent to Ameliorate, Prevent, and/or reverse Posttraumatic stress disorder (PTSD), Down‘s syndrome and Alzheimer‘s Disease. Patent USF#08B085_Echeverria, 2008 2. The use of cRaf-1 inhibitors to reverse Alzheimer‘s and Down‘s syndrome diseases. Patent application in process University of South Florida USF# 08B077_Echeverria. May 12th, 2008. 3. Cotinine for detection and diagnosis of conditions associated with A peptide aggregation. USF # 08B099, 2008 4. Beneficial Role of Sorafenib in Stroke and Other Neurological Disorders. USF# 09B071, 2010 Permanent 1. Materials and methods for diagnosis, prevention and/or treatment of stress disorders and conditions associated with abeta peptide aggregation. US 20100104504, filed April 29th,2010 The present application claims the benefit of U.S. Provisional Application Ser. No. 61/194,064, filed Sep. 24, 2008, and U.S. Provisional Application Ser. No. 61/099,746, filed Sep. 24, 2008

CONFERENCES

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October 2010. Invited Speaker. The BIT Life Sciences ‗8th Annual congress of International drug Discovery Science and Technology ―Cotinine: A Multiple Action Drug against Alzheimer‘s Disease‖. Beijing. China May-2010. Invited Speaker. Cotinine: ―Therapeutic implications in Alzheimer‘s Disease‖. Florida Association For Media in Education (FAME). American Chemical Society, Florida Section. Tampa, Fl. 2010 November-2009. Invited Professor. Faculty of Medicine. University San Sebastian. ―From Neuroscience to Clinical Neurology ―, three days Symposium. Concepcion, Chile. May-2009. Invited Speaker. Sorafenib restores working memory and decreases the expression of iNOS, CoxInstitute. University of South Florida. Tampa. FL, USA. November-2008. Invited Speaker. Faculty of Medicine. University San Sebastian. Department Seminars. ―Looking for New Therapeutic drugs against Alzheimer‘s disease Pathology‖. Concepcion, Chile. Sept-2008. Invited Speaker. Department of Chemistry. University of Miami. Department Seminars. ―Cotinine as a therapeutic drug against Alzheimer‘s disease pathology‖. Miami. FL, USA. April-2008. Invited Speaker. Dr. Dore‘s laboratory seminars. Sorafenib as a therapeutic drug against Alzheimer‘s disease Department of Anesthesiology and Critical Care. Faculty of Medicine. Johns Hopkins University. Baltimore, MD. USA.

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  

May-2007. Invited Speaker. University of South Florida. Seminar Neuroscience. Molecular Mechanisms of Alzheimer‘s disease pathology: Looking for new therapeutic targets. Tampa. FL, USA. Second speaker Web:http://hscvideo2.hsc.usf.edu/asxroot/com/ Biophysics/NSRP_Seminar_05_22_07.asx. 2006. Invited speaker. Merck-PA. Topic. Molecular Mechanisms of Alzheimer‘s disease. PA, USA. 1996. Invited speaker. University of Alcala, Faculty of Medicine. Topic. Cell signaling. Madrid. Spain. 1993. Invited speaker. Faculty of Agriculture. Plant Biotechnology. University of Concepcion, Chile.

TEACHING EXPERIENCE

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1999-2010 Mentoring graduate (3) and undergraduate (8) students in Biomedical Science Research. 1995-1999 Teaching Graduate Fellowship Seminars in Biochemistry to nursing students University of Concepcion, Chile 1991-1994 Teaching Graduate Fellowship Seminars in Biochemistry to Medicine, Nursing, and Obstetric students University of Concepcion, Chile

LANGUAGES English, Spanish, Italian, French and Portuguese (Only written comprehension)

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 9

BIOGRAPHICAL SKETCH Sebastiaan Engelborghs Title: University of Antwerp

Date of Birth: 21/09/1970

EDUCATION

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Institution and Location board certified neurologist and specialist in neurological revalidation

Degree MD, PhD.

Year Conferred

Scientific Field

Contact points Address: Universiteitsplein 1, 2610 Antwerp, Belgium RESEARCH AND PROFESSIONAL EXPERIENCE Dementia, BPSD, Alzheimer‘s disease, frontotemporal dementia, biomarkers

Professional Appointments Professor, senior consulting neurologist

Publications during last three years n=58 (2008-2009)

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 10

BIOGRAPHICAL SKETCH Carl L. Faingold Title: Professor, Ph.D. Southern Illinois University, School of Medicine, Dept. Pharmacology, Springfield, IL

Date of Birth: Feb.1, 1943

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EDUCATION Institution and Location

Degree

University of Illinois, Chicago, Illinois Northwestern University, Chicago, IL

B.S. Ph.D.

Year Conferred 1965 1970

Scientific Field Pharmacy Pharmacology

Contact points Address: P.O. Box 19629, (801 N. Rutledge) Springfield, Illinois 62794-9629

RESEARCH AND PROFESSIONAL EXPERIENCE Distinguished Professor of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 2009-Present Professor and Chairman Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 1995-Present Professor of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 1987-2009 Professor of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois, 1993-Present

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Professional Appointments Distinguished Professor of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 2009-Present Professor and Chairman Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 1995-Present Professor of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois, 1987-2009 Professor of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois, 1993-Present

Honors NIH. Traineeship in Pharmacology: 1965-1970 State of Missouri Post-doctoral Fellowship in Neuropharmacology-1970-1972 Wellcome Research Travel Grant - 1984 (supporting research at the Univ. of London, Institute of Psychiatry, Department of Neurology) Member United States Pharmacopeia (USP) Convention (9/4/2008) Excellence Through Commitment University-Level Outstanding Scholar Award (2009)

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Publications during last three years Long, C, Yang, L., Faingold, C.L and Evans, M.S., Excitatory amino acid receptor-mediated responses in periaqueductal gray neurons are increased during ethanol withdrawal, Neuropharmacology, 52:802-811, 2007. PMID: 17123553 Feng, H.-J., L. Yang and C. L. Faingold, Role of the amygdala in ethanol withdrawal seizures, Brain Res. 1141:65-73, 2007. PMID: 17289000 Feng HJ, Faingold, C.L. The effects of chronic ethanol administration on amygdala neuronal firing and ethanol withdrawal seizures. Neuropharmacology 55: 648-653, 2008. PMID: 18614185 Naritoku DK, Faingold CL, Development of a therapeutics curriculum to enhance knowledge of fourth year medical students about clinical uses and adverse effects of drugs. Teaching, Learning in Medicine 21(2):148-152, 2009. PMID: 19330694 N'Gouemo P, Faingold CL, Morad M, Calcium channel dysfunction inferior colliculus neurons of the genetically epilepsy-prone rat. Neuropharmacology 56(3):665-675, 2009. PMID: 19084544 N'Gouemo P, Yasuda RP, Faingold CL, Protein expression of small conductance calciumactivated potassium channels is altered in inferior colliculus neurons of the genetically epilepsy-prone rat. Brain Res 1270:107-111, 2009. PMID: 19254702 Tupal S, Faingold CL, Precipitous induction of audiogenic kindling by activation of adenylyl cyclase in the amygdala. Epilepsia 51(3):354-61, 2010 ID: 19674044 Uteshev, V.V., S. Tupal, Y. Mhaskar, and C. L. Faingold. Abnormal serotonin receptor expression in DBA/2 mice associated with susceptibility to sudden death due to respiratory arrest. Epilepsy Res. 88, pp. 183-188, 2010

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N'Gouemo, R. Yasuda, and C. L. Faingold. Seizure susceptibility is associated with altered protein expression of voltage-gated calcium channel subunits in inferior colliculus neurons of the genetically epilepsy-prone rat. Brain Res. 1308:153-157, 2010. Faingold, C.L., M. Randall, and S. Tupal. DBA/1 mice exhibit susceptibility to audiogenic seizures followed by sudden death associated with respiratory arrest. Epilepsy Behav. 17:436-440, 2010. Tupal, S. and Faingold, C.L. Inhibition of adenylyl cyclase in amygdala blocks the effect of audiogenic seizure kindling in genetically epilepsy-prone rats. Neuropharmacology, 59:107-111, 2010. Faingold, C.L. Brainstem networks: reticulo-cortical synchronization, Epilepsia 51 (Suppl. 5) Epub. 2010 Tupal, S. and Faingold, C.L. Audiogenic kindling induces plastic changes in the neuronal firing patterns in periaqueductal gray, Brain Res. 2011 (accepted). Vijaya Samineni, V., Louis S Premkumar, L.S., and Faingold, C.L. Post-ictal analgesia in genetically epilepsy-prone rats is induced by audiogenic seizures and involves cannabinoid receptors in the periaqueductal gray, Brain Res. 2011 (accepted).

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 11

BIOGRAPHICAL SKETCH Alon Friedman Title: The Department of Physiology and Neurobiology, The Department of Biomedical Engineering, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, BeerSheva

Date of Birth: October 9th, 1964

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EDUCATION Institution and Location

Degree

Ben-Gurion University of the Negev, Beer-Sheva, Medical Sciences. Ben-Gurion University of the Negev, Faculty of Health Sciences. Summa cum laude. Ben-Gurion University of the Negev, Department of Physiology, Faculty of Health Sciences Advisor: Professor Michael J. Gutnick "Active and Passive Properties of Neocortical Neurons and their Role in Determining Neuronal Firing Pattern"

B.Sc.

Year Conferred 7/85

M.D.

6/91

Ph.D.

1/92

Scientific Field

Contact points Address: The Department of Physiology and Neurobiology, Faculty of Health Sciences, BenGurion University of the Negev, Beer-Sheva, 84105, Israel.

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RESEARCH AND PROFESSIONAL EXPERIENCE

Professional Appointments 2011: Chair, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev. 2008-present:Associate Professor, Department of Physiology, Faculty of Health Sciences, Ben-Gurion University of the Negev. 2007-present:Associate-Chair, Department of Biomedical Engineering, Ben-Gurion University of the Negev. 2003-present:Senior Lecturer, Departments of Neurosurgery and Physiology, Soroka University Medical Center and Faculty of Health Sciences, Ben-Gurion University of the Negev. 7/02 – 04: Guest Scientist, Institute for Physiology, Humboldt University, Berlin. 1997: Lecturer, Departments of Neurosurgery and Physiology, Soroka University Medical Center and Faculty of Health Sciences, Ben-Gurion University of the Negev.

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Awards 2009: Mercator Program for Visiting Professorships at German Universities, Charite Medical University, Berlin, Germany. 2009: The Students Excellency award for teaching, Ben-Gurion University, Beer-Sheva, Israel. 2007: The Michael Prize for Epilepsy Research, The Michael Stiftung, Bonn, Germany. 2006: The Students Excellency award for teaching, Ben-Gurion University, Beer-Sheva, Israel. 2001-2: American Physicians Fellowship for Medicine in Israel, The APS Kass Award for Medical Research 2000:The Zigler prize for original research, The Bruce Rappaport Faculty of Medicine, Technion, Israeli Institute of Technology. 1997: The ―Teva‖ research prize for young investigators. 1997: Foulkes foundation research awards for original contribution of scientific research to medicine. 1991: The volunteer award, The Association for Civil Rights in Israel. 1986-1988: Goulton Award, Ben-Gurion University of the Negev, Israel. Support for graduate training. ‫‏‬ Fellowships 2002-3: Alexander von Humboldt Fellowship, Institute for Physiology, Humboldt University, Berlin. 1996-1997: The Charles Smith Post-Doctoral Fellowships 1988-1990: The Foulks Foundation Fellowship, London, UK, support for graduate training.

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Publications during last three years Randolf Klingebiel, Alon Friedman, Ilan Shelef and Jens P. Dreier. 2008, Focal cortical necrosis in a patient with high-grade ICA stenosis and status aurae migraenalis. Journal of Neurology Neurosurgery and Psychiatry, 79:89-90. Merav H Shamir, Orit Chi, Alon Friedman, Yael Shilo, Ram Reifen, and Limor Miara. 2008, Sub-occipital craniectomy in a lion (Panthera Leo) with occipital bone malformation and hypovitaminosis A. Zoo and Wild Animals Medicine. Journal of Zoo and Wildlife Medicine, 39(3): 455-459. Gabriel Zimmerman, Marleisje Njunting, Sebastian Ivens, Elsa Toner, Christopher J. Behrens, Miriam Gross, Hermona Soreq, Uwe Heinemann and Alon Friedman, 2008. Acetylcholine-Induced Seizure-like Activity and Cholinergic Modified Gene Expression in Chronically Epileptic Rats. European Journal of Neuroscience, 27(4):965-75. Alon Friedman, Daniela Kaufer and Uwe Heinemann, 2009. Blood-Brain Barrier BreakdownInducing Astrocytic Transformation: Novel Targets for the Prevention of Epilepsy. Epilepsy research, 85(2-3):142-9. Luisa P Cacheaux, Sebastian Ivens, Yaron David, Alexander J Lakhter, Guy Bar-Klein, Michael Shapira, Uwe Heinemann, Alon Friedman and Daniela Kaufer, 2009. Transcriptome profiling reveals TGF-beta signaling involvement in epileptogenesis. Journal of Neuroscience, 29(28): 8927-8935. Hadar Shalev, Yonatan Serlin and Alon Friedman, 2009. Breaching the Blood-Brain Barrier as a Gate to Psychiatric Disorder. Cardiovascular Psychiatry and Neurology. Ofer Prager, Yoash Chassidim, Chen Klein, Haviv Levi, Ilan Shelef and Alon Friedman, 2010. Dynamic in-vivo imaging of cerebral blood flow and blood-brain barrier permeability. Neuroimage, 49: 337-344. Yaron David, Luisa P Flores, Sebastian Ivens, Uwe Heinemann, Daniela Kaufer and Alon Friedman. 2009. Astrocytic dysfunction in epileptogenesis: consequences of altered potassium and glutamate buffering? Journal of Neuroscience, 29(34):10588-99. Marco Sifringer, Daniela Braita, Ulrike Weichelta, Gabriel Zimmerman, Stefanie Endesfeldera, Felix Brehmera, Clarissa von Haefen, Alon Friedman, Hermona Soreq, Ivo Bendixg, Bettina Gerstner, Ursula Felderhoff-Muesera, 2010. Erythropoietin attenuates hyperoxia-induced oxidative stress in the developing rat brain. Brain, behavior and immunity, (Epub ahead of print) 24:792-9. Epub 2009 Sep 1 Sebastian Ivens, Szendro Gabriel, Greenberg George, Alon Friedman and Ilan Shelef, 2010. Blood-brain barrier breakdown as a novel mechanism underlying cerebral hyperperfusion syndrome. Journal of Neurology, 257: 615-620. Dan Shlosberg, Mony Benifla, Daniela Kaufer and Alon Friedman. 2010. Blood-Brain Barrier Breakdown as a Therapeutic Target in Traumatic Brain Injury. Nature Reviews Neurology, 6: 393-404.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 12

BIOGRAPHICAL SKETCH Valantis Fyndanis Title: (a) Aristotle University of Thessaloniki, Greece (b) Technological Educational Institute of Epirus, Greece

Date of Birth: 20 November 1975

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EDUCATION Institution and Location

Degree

Aristotle University of Thessaloniki Aristotle University of Thessaloniki Aristotle University of Thessaloniki

Bachelor MA's PhD

Year Conferred

Scientific Field Linguistics Applied Linguistics Psycholinguistics

Contact points Address: Salaminos 3, 65403 Kavala, Greece

RESEARCH AND PROFESSIONAL EXPERIENCE

Professional Appointments Adjunct Professor (Univeristy of Trieste, Italy) (2007-2009); Scientific Collaborator (Technological Educational Institute of Epirus, Greece) (2010-2011)

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Publications during last three years

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Fyndanis, V. & Galiussi, F. (in press). Networks of canonical and mirror neurons and language teaching. Studies in Greek Linguistics, 31. (in Greek) Fyndanis, V. (2010). Short-term memory and language processing: Extending an interactive model to capture sentence-level data. Procedia-Social and Behavioral Sciences, 6, 70-71. Fyndanis, V., Varlokosta, S., & Tsapkini, K. (2010). Exploring wh-questions in agrammatism: Evidence from Greek. Journal of Neurolinguistics, 23, 644-662. Fyndanis, V. (2009). Tense, agreement and aspect in Greek agrammatism. Studies in Greek Linguistics, 29, 566-577. (in Greek) Manouilidou, C., Fyndanis, V., Kehayia, E., & Ralli, A. (2009). Processing thematic features: From Derivation to Compounding. Proceedings of the 8th International Conference on Greek Linguistics. University of Ioannina. Available on-line: http://www.linguistuoi.gr/cd_web/docs/english/024_manouilidouICGL08.pdf.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 13

BIOGRAPHICAL SKETCH Rigoberto Gonzalez Pina Title: Laboratorio de Neuroplasticidad, Instituto Nacional de Rehabilitacion

Date of Birth: 7 Apr, 1965

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EDUCATION Institution and Location

Degree

Universidad Nacional Autonoma de Mexico

Ph. D.

Year Conferred

Scientific Field Science‘s Faculty

Contact points Address: Calz. Mexico-Xochimilco 289 Col Arenal de Guadalupe C.P. 14389 Mexico City MEXICO

RESEARCH AND PROFESSIONAL EXPERIENCE Neurology and Neurosurgery‘s National Institute. Associated Researcher Rehabilitation‘s National Institute. Senior Researcher Rehabilitation‘s Superior School. Professor (1 Documental research, 2 Biostatistics and 3 Scientific method) University of the Americas. Professor (Genetics)

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Professional Appointments 11 Bachelor‘s thesis 2 Master‘s thesis 24 international papers 6 book chapters Honors Member of the Researcher‘s National System 2 bursaries granted from the Science and Technology´s National Council (CONACYT)

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Publications Last 3 Years Bueno-Nava A, Gonzalez-Pina R, Avila-Luna A, Alfaro-Rodriguez A. Paradigm of negative feedback via long-loop in the striatal dopamine release modulation in the rat Rev Neurol. 2011; 52(6):371-7. Bueno-Nava A, Gonzalez-Pina R, Alfaro-Rodriguez A, Nekrassov-Protasova V, DurandRivera A, Montes S, Ayala-Guerrero F. Recovery of motor deficit, cerebellar serotonin and lipid peroxidation levels in the cortex of injured rats. Neurochem Res. 2010;35(10):1538-45. Bueno-Nava A, Gonzalez-Pina R, Alfaro-Rodriguez A. Iron-dextran injection into the substantia nigra in rats decreases striatal dopamine content ipsilateral to the injury site and impairs motor function. Metab Brain Dis. 2010;25(2):235-9. Durand-Rivera JA, Manzano-Martínez E, González-Piña R. Is cochlear processing involved in language disorders? Rev Neurol. 2009;48(12):639-44. Alfaro-Rodríguez A, González-Piña R, Arch-Tirado E, Carrasco-Portugal M, Pérez-Guillé B, Soriano-Rosales RE, Padilla-Martin K, Uribe-Escamilla R, Labra-Ruiz N. Neuroprotective effects of carbamazepine on sleep patterns and head and body shakes in kainic acid-treated rats. Chem Biol Interact. 2009;180(3):376-82.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 14

BIOGRAPHICAL SKETCH Sunghoi Hong Title: Korea University

Date of Birth: October 20, 1969

EDUCATION Institution and Location

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Korea University Korea University Korea University

Degree Ph.D. M.S. B.S.

Year Conferred

Scientific Field

2001 1996 1994

Contact points Address: San1, Jeongneung-dong, Seongbuk-gu, Seoul 136-701, South Korea

RESEARCH AND PROFESSIONAL EXPERIENCE 1. Associate Professor: College of Health Science, Korea University (2010 ~ Present) 2. Assistant Professor: College of Health Science, Korea University (2009 ~ 2010) 3. Post-doctoral Fellow: Harvard Medical School, Harvard University (2004 ~ 2009) 4. Research Professor: School of Life Science and Biotechnology, Korea University (2003 ~ 2004) 5. Lecturer: College of Life Environment and Science, Konkuk University (2003) 6. Post-doctoral Fellow: Graduate School of Biotechnology, Korea University (2001 ~ 2003 7. Researcher: Seoul Clinical Laboratory, Seoul Medical Science Institute (1996 ~ 1998)

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Professional Appointments He has been appointed Korea ALS Association (KALSA) Committee of Board of Directors from November 2000 to 2006

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Biography Dr. Hong completed his doctorate from the graduate program in molecular biology at the Korea University, South Korea in 2001. The goal of his research was to explore the function of ataxin-1, the SCA1 gene product, in spinocerebellar ataxia type 1 (SCA1) diseases. The main objective of the research was identification of several ataxin-1-interacting proteins in yeast two-hybrid screen, and then elucidating its function in cell culture system and transgenic mice systems. After his pathogenesis study of SCA1 disease, he joined the Institute of Life Science at Korea University as a research professor in 2003, where he directed his research to both cell culture system and animal model-based system with transgenic mice. He joined Drs. Kwang-Soo Kim and Ole Isacson‘s laboratories of McLean Hospital and Harvard Stem Cell Institute at Harvard Medical School in the spring of 2004 as a post-doctoral fellow. His research project was involved in inducing enriched dopaminergic neurons from human embryonic stem (hES) cells as well as mouse ES cells. The ultimate goal was the pathogenesis and development of cell-based therapies for Parkinson's disease. After his post-doctor fellowship, he joined the Department of Biomedical Science at Korea University in 2009 March as a professor, where he is applying the stem cells, including adults stem cells, embryonic stem cells, and induced pluripotent stem cells etc., to development of therapies for neurodegenerative diseases, such as Alzheimer‘s disease (AD), Parkionson‘s disease (PD), and SCA1 disease etc. It is expected that this work will contribute to molecular and cellular pathogenesis and the development of novel cell-based therapies for the neurodegenerative diseases.

Publications during last three years Sunghoi Hong and Seongman Kang. 2011. Prediction of personalized drugs based on genetic variations provided by DNA sequencing technologies. Current Pharmacautical Biotechnology. Â (in revision). Soyoen Lee, Sunghoi Hong, Sungsu Kim and Seongman Kang. 2011 (Feb 22). Ataxin-1 occupies the promoter region of E-cadherin in vivo and activates CtBP2-repressed promoter. Biochimica et Biophysica Acta-Molecular Cell Research (BBAMCR). Seongman Kang and Sunghoi Hong*. 2010 (December). SUMO-1 interacts with mutant ataxin-1 and colocalizes in Purkinje cells of SCA1 transgeneic mice. Archives Italiennes de Biologie 148:351-363 *Corresponding author. Sangmi Chung, Amanda Leung, Back-Soo Han, Mi-Yoon Chang, Jung-Il Moon, ChunHyung Kim, Sunghoi Hong, Jan Pruszak, Ole Isacson, and Kwang-Soo Kim 2009 (December 4). Wnt1-lmx1a forms a novel autoregulatory loop and controls midbrain dopaminergic differentiation synergistically with the SHH-FoxA2 pathway. Cell Stem Cell. 5:1-13.

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Dong-Youn Hwang, Sunghoi Hong, Joo-Won Jeong, Sangdun Choi, Hansoo Kim, Jangwoo Kim, and Kwang-Soo Kim 2009 (September 24). VMAT2 and DAT are molecular targets of Pitx3 in the ventral midbrain dopamine neurons. Journal of Neurochemistry. 111:1201-1212. Man Ki Song, Jun Chang, Yeongjin Hong, Sunghoi Hong, and Suhng Wook Kim. 2009 (July 22) Direct Multiplex Reverse Transcription-Nested PCR Detection of Influenza Viruses Without RNA Purification. Journal Microbiology and Biotechnology. 19(11):1470-1474. Seongman Kang and  Sunghoi Hong*. 2009 (June 30). Molecular pathogenesis of Spinocerebellar ataxia type 1 disease. Molecules and Cells. 27(6): 621-627. *Corresponding author. Seok Jong Hong, Hyun Jin Choi, Sunghoi Hong, Youngbum Huh, Han Chae and Kwang-Soo Kim. 2008 (September). Transcription factor GATA3 regulates the transcriptional activity dopamine-β hydroxylase by interacting with Sp1 and AP4. Neurochemical Research. 33(9):1821-1831. Sunghoi Hong*, Soyoen Lee*, and Seongman Kang. 2008 (August 8). The ubiquitinconjugating enzyme UbcH6 regulates the transcriptional repression activity of the SCA1 gene product ataxin-1. Biochemical and Biophysical Research Communication (BBRC). 372(4):735-740. *Both authors equally contributed to this work. Sunghoi Hong, Soyoen Lee, Ssang-Goo Cho and Seongman Kang. 2008 (June 27). UbcH6 interacts and ubiquitinates the SCA1 gene product ataxin-1. Biochemical and Biophysical Research Communication (BBRC). 371(2):256-260. Seok Jong Hong, Han Chae, Thomas Lardaro, Sunghoi Hong and Kwang-Soo Kim. 2008 (April 11 ). Trim11 increases expression of dopamine-β hydroxylase gene by interacting with Phox2b. Biochemical and Biophysical Research Communication (BBRC). 368(3):650-655. Dongwon Choi, Sun-Joo Lee, Sunghoi Hong, Ik-Hwan Kim, and Seongman Kang. 2008 (March 13). Prohibitin interacts with RNF2 and regulates E2F1 function via dual pathways. Oncogene. 27(12):1716-1725. Sunghoi Hong, Un Jung Kang, Ole Isacson and Kwang-Soo Kim 2008 (January). Neural precursors derived from human embryonic stem cells maintain long-term proliferation without losing the potential to differentiate into all three neural lineages, including dopaminergic neurons. Journal of Neurochemistry. 104(2):316-324. Miles Cunningham, Rachael Donalds, William A. Carlezon Jr., Sunghoi Hong, Dae-Sung Kim, Dong-Wook Kim and Kwang-Soo Kim. 2007 (Oct 29). Antidepressant Effect of Stem Cell-Derived Monoaminergic Grafts. NeuroReport. 18(16):1663-1667. Sunghoi Hong, Dong-Youn Hwang, Soonsang Yoon, Ali Ramezani, Robert G. Hawley, Ole Isacson and Kwang-Soo Kim 2007 (September). Functional analysis of various promoters in lentiviral vectors at different stages of in vitro differentiation of mouse embryonic stem cells. Molecular Therapy. 15(9): 1630-1639. (This article was highlighted in Biotechniques• 43:547,2007) Eva Hedlund, Jan Pruszak, Angel Viňuela, Andrew Ferree, Sunghoi Hong, Ole Isacson and Kwang-Soo Kim. 2007 (May). Selection of embryonic stem cells-derived enhanced green fluorescence protein-positive dopamine neurons using the tyrosine hydroxylase promoter is confounded by reporter gene expression in immature cell populations. Stem Cells. 25(5):1126-1135.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 15

BIOGRAPHICAL SKETCH Kazuaki Inoue Title: MD, PhD. Showa University Fujigaoka Hospital Division of Gastroenterology

Date of Birth: 5th Dec 1959

EDUCATION

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Institution and Location

Degree

Showa University School of Medicine Showa University Postgraduate School Awarded the degree of MD Research work was supervised by Professor Ikuo Honma

Year Conferred

Scientific Field

1982- 1986 1988 – 1990

Contact points Address: 1-30 Fujigoka Aoba-ku Yokohama 227-8501 Japan RESEARCH AND PROFESSIONAL EXPERIENCE 1990– 1992: Assistant Professor at the Showa University, School of Medicine 1990–1994: Assistant Professor at the Division of Gastroenterology, Showa UniversityFujigaoka Hospital 1994–1996: Assistant Professor at the Division of Emergency Medicine, Showa University Fujigaoka Hospital 1996 – 1999: Research Associate, Department of Microbiology and Cell Biology, The Tokyo Metropolitan Institute of Medical Science

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1999 - present: Visiting researcher, Department of Microbiology and Cell Biology, The Tokyo Metropolitan Institute of Medical Science 1999–2001: Assistant Professor, Division of Gastroenterology, Showa University Fujigaoka Hospital 2001 – present: Associate Professor, Division of Gastroenterology, Showa University Fujigaoka Hospital

Professional Appointments 2001 –present: Associate Professor, Division of Gastroenterology, Showa University Fujigaoka Hospital 1992 –present: Member of research group of Ministry of Health,Labour and Welfare (Fulminant hepatic failure) 2010 - present: Member of research group of Ministry of Health, Labour and Welfare (New treatment for chronic hepatitis C)

Honors The 17th Promotion Award of the Japanese Society of Gastroenterology, 2004 Promotion Award of Alumni Association of Showa University, 2004 The16th Kamijo Academic Award founded by Showa University, 2004 The 1st Chugai Award of the Japan Society ofHepatology, 2008

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Publications Last 3 Years Inoue K, Kourin A, Yamada M, Watanabe T, Yoshiba M. Artificial liver support system using huge buffer volumes removes significant glutamine from patient plasma with good clinical effects. J Hepatol 2008; 48 (Suppl. 2): S86 Inoue K, Watanabe T, Yoshiba M. Host factor targeting therapy gives a new insight to intractable chronic hepatitis C. J Hepatol 2008; 48 (Suppl. 2): S318-S319 Inoue K, Yoshiba M. Huge-volume buffer of artificial liver support removes significant glutamine from patient plasma associated with good clinical effects. Gastroenterology 2008; 134 (4) Suppl. 1; A-759-A760 Inoue K, Yamada, M, Yoshiba M. Online HDF system with good removal capacity of glutamine brings good clinical effect. The International Journal of Artificial Organs 2008; 31: 587 Inoue K, Matsuda C, Watanabe T, Yoshiba M, Kohara M. Cyclophilins are essential host factors for HCV RNA replication and potent cyclophilin inhibitors are potential antiHCV drugs. Hepatology 2008; 48 (4) Suppl.; 385A Inoue K, Kourin A, Watanabe T, Yamada M, Yasuda H, Yoshiba M. Plasma exchange in combination with online-hemodiafiltration as a promising method for purifying the blood of fulminant heptitis patients. Hepatol Res 2008; 38 (Suppl. 1); S46-S51

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Ogawa O, Yoshikumi H, Maruoka N, Hashimoto Y, Kishimoto Y, Tsunamasa W, Kuroki Y, Yasuda H, Endo Y, Inoue K, Yoshiba M. Predicting the success of endoscopic transpapillary gallbladder drainage for patients with acute cholecystitis during pretreatment evaluation. Can J Gastroenterol 2008; 22(8): 681-685 Inoue K, Watanabe T, Yamada M, Yoshikumi H, Ogawa O, Yoshiba M. Efficacy of InterferonCombined With Cyclosporine Induction and Intensified Therapy for Retreatment of Chronnic Hepatitis C. Transplant Proc 2009; 41 (1): 246-249 Inoue K, Kourin A, Watanabe T, Yamada M, Yoshiba M. Artificial Liver Support System Using Large Buffer Volumes Removes Significant Glutamine and Is an Ideal Bridge to Liver Transplantation. Transplant Proc 2009; 41 (1): 259-261 Inoue K, Watanabe T, Yoshiba M, Kohara M. Cyclophilins are essential host factors for HCV replication: The required level varies with HCV clone. J Hepatol 2009; 50(Suppl.1); S126 Hirata Y, Sudoh, M, Tsukuda T, Ikeda K, Taguchi R, Inoue K, Yoshiba M, Kohara M.A newly synthesized serine palmitoyl transferase inhibitor, NA 808, has the strong effect ot hepatitis C virusin vitro andin vivo. J Hepatol 2009; 50(Suppl.1); S344

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 16

BIOGRAPHICAL SKETCH Felix Junyent Herena Title: PhD in Biology Univesritat de Barcelona, Centro de investigaciones biomédicas en red en enfermedades neurodegenerativas (CIBRENED)

Date of Birth: 12/04/1981

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EDUCATION Institution and Location PhD in Biology

Degree

Year Conferred

Scientific Field

Contact points Address: Avda/Diagonal 643, Facultat de Farmacia, Unitat de Farmacologia, UB. 08028. Barcelona, Spain

RESEARCH AND PROFESSIONAL EXPERIENCE Research in neurosciences, specifically in molecular mechanisms of neuronal death in neurodegenerative disease.

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Professional Appointments 2004-2008. Pre-doctoral researcher in Cell Biology Department, Faculty of Biology, University of Barcelona 2008-Now. Postdoctoral researcher in Centro de Investigaciones Biomédicas en Red en Enfermedades Neurodegenerativas (CIBERNED). 2009-Now. Associate Professor of Biochemistry in University Rovira I Virgili (Reus, Spain).

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Publications during last three years 1. Junyent F, Porquet D, de Lemos L, Romero R, Utrera J, Camins A, Pallás M, Auladell C. Decrease of calbindin-d28k, calretinin and parvalbumin by taurine treatment does not induce major susceptibility to kainic acid. J Neurosci Res. 2011; 89(7): 1043-51. 2. Pizarro JG, Folch J, Junyent F, Verdaguer E, Auladell C, Beas-Zarate C, Pallás M, Camins A. Antiapoptotic effects of roscovitine on camptothecin-induced DNA damage in neuroblastoma cells. Apoptosis. 2011; 16(5): 536-50. 3. Sureda FX, Junyent F, Verdaguer E, Auladell C, Pelegrà C, Vilaplana J, Folch J, Canudas AM, Zarate CB, Pallás M, Camins A. Antiapoptotic drugs: a therapheutic strategy for the prevention of neurodegenerative diseases. Curr Pharm Des. 2011; 17(3): 230-45. 4. Junyent F, de Lemos L, Verdaguer E, Folch J, Ferrer I, Ortuňo-Sahagŭn D, Beas-Zárate C, Romero R, Pallás M, Auladell C, Camins A. Gene expresion profile in JNK3 null mice: a novel specific activation of the PI3K/AKT pathway. J Neurochem. 2011; 117(2): 244-52. 5. Pizarro JG, Verdaguer E, Ancrenaz V, Junyent F, Sureda FX, Pallás M, Folch J, Camins A. Resveratrol inhibits proliferation and promotes apoptosis of neuroblastoma cells: role of sirtuin 1. Neurochem Res. 2011; 36(2):187-94. 6. Ortuño-Sahagún D, Rivera-Cervantes MC, Gudiño-Cabrera G, Junyent F, Verdaguer E, Auladell C, Pallás M, Camins A, Beas-Zárate C. Microarray analysis of rat hippocampus exposed to excitotoxicity: Reversal Na(+)/Ca(2+) exchanger NCX3 is overexpressed in glial cells. Hippocampus. 2011; doi: 10.1002/hipo.20869. 7. Viayna E, Gómez T, Galdeano C, Ramírez L, Ratia M, Badia A, Clos MV, Verdaguer E, Junyent F, Camins A, Pallà s M, Bartolini M, Mancini F, Andrisano V, Arce MP, RodrÍguez-Franco MI, Bidon-Chanal A, Luque FJ, Camps P, Muñoz-Torrero D. Novel huprine derivates with inhibitory activity toward b-amyloid aggregation and formation as diseasemodifying anti-Alzheimer drug candidates. ChemMedChem. 2010; 5(11): 1855-70. 8. Junyent F, Alvira D, Yeste-Velasco M, de la Torre AV, Beas-Zárate C, Sureda FX, Folch J, Pallás M, Camins A, Verdaguer E. Prosurvival role of JAK/STAT and Akt signalling pathways in MPP+-induced apoptosis in neurons. Neurochem Int. 2010; 57(7): 774-82. 9. Camins A, Sureda FX, Junyent F, Verdaguer E, Folch J, Pelegri C, Vilaplana J, BeasZarate C, Pallas M. Sirtuin activators: designing molecules to extend life span. Biochim Biophys Acta. 2010; 1799(10-12): 740-9. 10. de Lemos L, Junyent F, Verdaguer E, Folch J, Romero R, Pallás M, Ferrer I, Auladell C, Camins A. Differences in activation of ERK1/2 and p38 kinase in Jnk3 null mice following KA treatment. J Neurochem. 2010; 114(5): 1315-22. 11. Camins A, Pizarro JG, Alvira D, Gutierrez-Cuesta J, de la Torre AV, Folch J, Sureda FX, Verdaguer E, Junyent F, Jordán J, Ferrer I, Pallás M. Activation of ataxia telangiectasia

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mutated under experimental models and human Parkinson‘s disease. Cell Mol Life Sci. 2010; 67(22): 3865-82. 12. Tajes M, Gutierrez-Cuesta J, Folch J, Ortuño-Sahagún D, Verdaguer E, Jiménez A, Junyent F, Lau A, Camins A, Pallás M. Neuroprotective role of intermittent fasting in senescence-accelerated mice P8 (SAMP8). Exp Gerontol. 2010; 45(9): 702-10. 13. Camins A, Sureda FX, Junyent F, Verdaguer E, Folch J, Beas-Zárate C, Pallás M. An overview of investigational antiapoptotic drugs with potential application for the treatment of neurodegenerative disorders. Expert Opin Investig Drugs. 2010; 19(5): 587604. 14. Pizarro JG, Folch J, de la Torre AV, Junyent F, Verdaguer E, Jordán J, Pallás M, Camins A. ATM is envolved in cell-cycle control through the regulation of retinoblastoma proteÃna phosphorylation. J Cell Biochem. 2010; 110(1):210-8. 15. Junyent F, de Lemos L, Utrera J, Paco S, Aguado F, Camins A, Pallas M, Romero R, Auladell C. Content and traffic of taurine in hippocampal reactive astrocytes. Hippocampus. 2011; 21(2): 185-97. 16. Pizarro JG, Junyent F, Verdaguer E, Jordán J, Beas-Zárate C, Pallas M, Camins A, Folch J. Effects of MPP+ on the molecular pathways involved in cell cycle control in B65 neuroblastoma cells. Pharmacol Res. 2010; 61(5): 391-9. 17. Duran-Vilaregut J, del Valle J, Manich G, Junyent F, Camins A, Pallas M, Pelegri C, Vilaplana J. Systemic administration of 3-nitropropionic acid points out different role for active caspase-3 in neurons and astrocytes. Neurochem Int. 2010; 56(3): 443-50. 18. Utrera J, Junyent F, de Lemos L, Pallás M, Camins A, Romero R, Auladell C. Tau hyperphosphorylation and axonal damage induced by N,N-diethyldithiocarbamate (DEDTC) treatment along late postnatal development is followed by a rescue during adulthood. J Neurosci Res. 2010; 88(5): 1083-93. 19. Camins A, Verdaguer E, Junyent F, Yeste-Velasco M, Pelegri C, Vilaplana J, Pallas M. Potential mechanisms involved in the prevention of neurodegenerative diseases by lithium. CNS Neurosci Ther. 2009; 15(4): 333-44. 20. Junyent F, Utrera J, Camins A, Pallas M, Romero R, Auladell C. Synthesis, uptake and release of taurine in astrocytes treated with 8-Br-cAMP. Neurosci Lett. 2009; 467(3): 199-202. 21. Camins A, Crespo-Biel N, Junyent F, Verdaguer E, Canudas AM, Pallà s M. Calpains as a target for therapy of neurodegenerative diseases: putative role of lithium. Curr Drug Metab. 2009; 10(5):433-47. 22. Junyent F, Romero R, de Lemos L, Utrera J, Camins A, Pallás M, Auladell C. Taurine treatments inhibits CaMKII activity and modulates the presence of calbindin-d28k, calretinin and parvalbumin in the brain. J Neurosci Res. 2010; 88(1): 136-42. 23. Pizarro JG, Folch J, Vazquez de la Torre A, Verdaguer E, Junyent F, Jordan J, Pallas M, Camins A. Oxidative stress-induced DNA damage and cell cycle regulation in B65 dopaminergic cell line. Free Radic Res. 2009; 43(10): 985-94. 2.- Junyent F, Utrera J, Romero R, Pallás M, Camins A, Duque D, Auladell C. Prevention of epilepsy by taurine treatments in mice experimental model. J Neurosci Res. 2009; 87(6): 1500-8.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 17

BIOGRAPHICAL SKETCH Anna Hrabovska Title: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Bratislava, Slovakia

Date of Birth: June 29th, 1976

EDUCATION

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Institution and Location Faculty of Pharmacy Faculty of Pharmacy Faculty of Pharmacy

Degree Master of Pharmacy PharmD PhD

Year Conferred 1999) 2001 2005

Scientific Field pharmacology pharmaceutical chemistry

Contact points Address: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Odbojarov 10, 832 32 Bratislava, Slovakia

RESEARCH AND PROFESSIONAL EXPERIENCE Comenius University, Faculty of Pharmacy, Dept. of Pharmacology and Toxicology; Bratislava, Slovakia (July 2009 – present)

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Professional Appointments Associate Professor  Head of the lab of Neurobiology, with special scientific interest in the cholinergic system – Manage a team of researchers, technicians and students – Manage and supervise the research projects  Involved in teaching activities (lectures and seminars) in Slovak and English study programs – In the subjects of physiology, pathology, Â pharmacology and toxicology State institute for drug control; Bratislava, Slovakia (Sept 2009 – present) Full member of the Subcommittee for generics (since 2010) 

Participate in the assessment of EU registrations of generic drugs and in generic drug politics in Slovakia

CNRS UMR 8544, Ecole Normale Supérieure; Paris, France; Lab of prof. J. Massoulié, PhD; supervised by E. Krejci, PhD (March 2009 – May 2009) Post-doctoral researcher

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and UFR Biomédicale Paris 5, INSERM U686, Biologie des Jonctions Neuromusculaires; Paris, France; Lab of prof. C. Legay, PhD; supervised by E. Krejci, PhD (Oct 2005 – June 2009) Post-doctoral researcher • •





Developed a detection tool for the congenital myastenic syndrome in human patients, which is used in practice at the Hôpital Pitié Salpêtrière in Paris, France Suggested, designed and developed a novel strategy for generation of specific and selective monoclonal antibodies against weak antigens. The invented method has been submitted for patent granting Participated in research of the neuromuscular junction (NMJ); determining basic characteristics of NMJ in wild-type and genetically modified mice (with alteration of different molecular forms of cholinesterases) Developed an efficient tool to detect and quantify different heterooligomers of cholinesterases and anchoring proteins

Charles University, 1st Faculty of Medicine, Institute of Physiology; Prague, Czech Republic; Lab of J. MysliveÄ•ek, PhD (April 2005 – May 2005)

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Visiting researcher • Determined the adaptation changes of different receptor systems (dopaminergic, adrenergic) in brain of acetylcholinesterase knock-out mice Centre de Recherches du Service de Sante des Armees, Toxicology Dept.; La Tronche, France; Lab of prof. P. Masson, PharmD., Sc.D. (May 2004 – July 2004) Visiting student • •

Worked on the steady-state kinetics of benzoylcholine and its N-alkyl homologues by recombinant rat butyrylcholinesterase; performed docking studies Participated in the discovery of the oscillations and a lag phase in the pre-steady-state kinetics of cholinesterases

University of Nebraska Medical Center, Eppley Institute; Omaha, NE, USA; Lab of prof. O. Lockridge, PhD (Oct 2001 – Dec 2003)> Visiting researcher • •



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Participated in research dealing with development of therapeutic reagents to prevent toxicity of nerve agents and treatment of toxicity of organophosphorus pesticides Performed gene therapy of acetylcholinesterase knock-out mice including plasmid cloning, adeno-associated virus preparation, tissue culturing, viral titration and in vivo viral delivery at multiple sites (i.m., i.v., s.c, i.c.) Studied changes in cholinergic and dopaminergic pathways in acetylcholinesterase knock-out mice including behavioral analyses, receptor binding assays (by Western analysis and Radioligand binding) and toxicological studies Prepared and purified recombinant rat butyrylcholinesterase

Comenius University, Faculty of Pharmacy, Dept. of Cell and Mol. Biology of Drugs; Bratislava, Slovakia (Sept 1999 – Jun 2001; Jan 2005 – Oct 2005) Scientific researcher • •

Performed research related to the study of xenobiotic biotransformation; Supported student research in related research areas; tutored master students, taught biochemistry, pathobiochemistry and xenobiochemistry, reviewed student thesis; one of the undergraduate student‘s oral presentation was awarded best presentation at the National Student Conference in Bratislava (April 2006) as well as at the International Student conference in Prague (May 2006)

Honors 2010-2012 – collaborative project between France and Slovakia supported by French and Slovak governments (APVV/Stefanik grant) 2010-2012 – collaborative project between Czech Republic and Slovakia supported by Czech and Slovak governments (APVV grant)

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2010 – selected for publication in the Marrquis‘ Who is Who in the world 2008-2009 – post-doctoral fellowship from Agence Nationale de la Recherche (ANR Neuroscience) 2005-2007 – post-doctoral fellowship from Association Francaise contre les Myopathies (AFM) for the project: Acetylcholinesterase deficient Congenital Myasthenic Syndrome: New strategy to quantify AChE in one synapse 2005-2007 – research grant VEGA 1/2271/05 awarded by the Ministry of Education of Slovak Republic 2006-2007 – travel Slovak and Czech exchannge grant from Ministry of Education of Slovak Republic and Ministry of Education of Czech Republic 2004-2005 – research grant from Comenius UUniversity for PhD Student 2004 – winning presentation at the Nationaal PhD Student Conference in Bratislava 2004 – mobility international grant for PhD students from Comenius University in Bratislava; supporting a research visit at the Centre de Recherches du Service de Sante des Armees; Toxicology Dept.; La Tronche, France, in the laboratory of prof. Patrick Masson 2001-2002 – supplementary grant for a reseearch stay in USA from American Czech and Slovak Society 2000-2001 – research grant from Comenius UUniversity for PhD students 2000-2001 – research grant from Faculty off Pharmacy in Bratislava for PhD students

Publications during last three years

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Bernard V, Girard E, Hrabovska A, Camp S, Taylor P, Plaud B, Krejci E: Disposition and Functions of Acetylcholinesterase Molecular forms at the Neuromuscular Junction. Mol. Cell Neurosci. 2011; 46(1): 272-281. 1) Hrabovska A, Bernard V, Krejci E: A novel system for the efficient generation of antibodies following  immunization of unique knockout mouse strains. PLoS ONE 2010;  5(9): e12892. 2) Hrabovská A, FarÁr V, Bernard V, Duysen EG, Brabec J, Lockridge O, MysliveÄ•ek J: Drastic decrease in dopamine receptor levels in the striatum of acetylcholinesterase knock-out mouse. Chem. Biol. Interact. 2010; 183(1): 194-201. 3) Dobbertin A, Hrabovska A, Dembele K, Camp S, Taylor P, Krejci E, Bernard V: Targeting of Acetylcholinesterase in Neurons in vivo: A Dual Processing Function for the Proline-rich Membrane Anchor Subunit and the Attachment Domain on the Catalytic Subunit. J. Neurosci. 2009; 29(14): 4519-4530. 4) MysliveÄ•ek J, Hrabovská A: Dopamine receptors regulation by non-dopaminergic mechanisms. In: Dopamine Research Advances. Akiyama Watanabe, Ed.,  Nova Science Publishers, Inc., Hauppauge, NY, USA, 2008.

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Chapter 18

BIOGRAPHICAL SKETCH Masahisa Katsuno Title: M.D., Ph.D. Medicine

Date of Birth: February 24th, 1971

Contact points [email protected]

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH AND PROFESSIONAL EXPERIENCE Molecular science and clinical neurology

Professional Appointments Associate Professor

Publications during last three years Katsuno M, Banno H, Suzuki K, et al. Efficacy and safety of leuprorelin in patients with spinal and bulbar muscular atrophy (JASMITT study): a multicentre, randomised, double-blind, placebo-controlled trial. Lancet Neurol. 9: 875-884, 2010. Katsuno M, Adachi H, Minamiyama M, et al. Disrupted TGF-beta signaling in spinal and bulbar muscular atrophy. J Neurosci. 30: 5702-5712, 2010. Katsuno M, Adachi H, Sobue G. Getting a handle on Huntington's disease: the case for cholesterol. Nat Med. 15: 253-254, 2009.

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Chapter 19

BIOGRAPHICAL SKETCH Michelle Y. Kibby Title: PhD

Date of Birth:

EDUCATION Institution and Location

Degree

Year Conferred

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

PhD

Scientific Field Clinical Psychology with specialized training in childclinical neuropsychology

Contact points Address: Southern Illinois University-Carbondale Dept. of Psychology LSII, Room 281 Carbondale, IL 62901

RESEARCH AND PROFESSIONAL EXPERIENCE 2 NIH funded grants, 19 articles in peer-reviewed journals, 2 book chapters, over 80 conference presentations; populations of interest are dyslexia and ADHD My areas of expertise include child neuropsychology and developmental cognitive neuroscience. I began this concentration by double majoring in neuropsychology and child clinical psychology in graduate school. I then continued my emphasis in child neuro-

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psychology throughout my internship and two post-doctoral fellowships. My first postdoctoral fellowship was with Morris Cohen where I studied memory functioning in dyslexia and ADHD. My second post-doctoral fellowship was under George W. Hynd where I trained in structural, quantitative MRI as applied to dyslexia and ADHD.

Professional Appointments Professional Appointments: Associate Professor in Psychology, with cross-appointment to the SIU School of Medicine

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Publications during last three years Mesman, G. R. & Kibby, M.Y. (2011). Examining multiple theories‘ contribution to orthographic functioning. Journal of Learning Disabilities, 44, 50-62. Kibby, M.Y., Kroese, J.M., Krebbs, H., Hill, C.E., & Hynd, G.W. (2009). The pars triangularis in dyslexia and ADHD: A comprehensive approach. Brain and Language, 111, 46-54. Kibby, M.Y. (2009). Memory functioning in dyslexia: An analysis using two clinical memory measures. Archives of Clinical Neuropsychology, 24, 245-254. Kibby, M.Y. (2009). There are Multiple Contributors to the Verbal Short-term Memory Deficit in Children with Developmental Reading Disabilities. Child Neuropsychology, 15, 485-506. Kibby, M.Y., Pavawalla, S.P., Fancher, J.B., Naillon, A.J., & Hynd, G.W. (2009). The relationship between cerebral hemisphere volume and receptive language functioning in dyslexia and Attention-Deficit/Hyperactivity Disorder. Journal of Child Neurology, 24, 438-448. Kibby, M.Y. & Cohen, M.J. (2008). Memory functioning in children with reading disabilities and/or Attention-Deficit/Hyperactivity Disorder: A clinical investigation of their working memory and long-term memory functioning. Child Neuropsychology, 14, 525-546. Kibby, M.Y., Fancher, J.B., Markanen, R., & Hynd, G.W. (2008). A quantitative MRI analysis of the cerebellar deficit hypothesis of dyslexia. Journal of Child Neurology, 23, 368-80.

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Chapter 20

BIOGRAPHICAL SKETCH Philip C. Ko Title: Vanderbilt University

Date of Birth: 1978

EDUCATION

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Institution and Location Vanderbilt University

Degree

Year Conferred

Ph.D.

2010

Scientific Field

Contact points Address: Dept of Psychology, Vanderbilt University, 111 21st Avenue South, Nashville, TN, 37203

Professional Appointments •

2010 – present: Senior Lecturer, Department of Psychology, Vanderbilt University, Nashville TN

Publications during last three years Ko, P.C. & Ally, B.A. (in press) Visual cognition in Alzheimer‘s disease and its functional implications. In Alzheimer‘s Disease, Book 1 (working title), InTech.

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Ko, P.C. & Seiffert, A.E. (2009) Updating objects in visual short-term memory is featureselective. Memory and Cognition, 37(6), 909 – 923. Wilkinson, D.T., Ko, P.C., Wiriadjaja, A., Kilduff, P., McGlinchey, R. & Milberg, W.P. (2009) Unilateral damage to the right cerebral hemisphere disrupts the apprehension of whole faces and their component parts. Neuropsychologia, 47(7), 1701 – 11. Wilkinson, D.T., Ko, P.C., Milberg, W.P., & McGlinchey, R. (2008) Impaired search for orientation but not color in hemi-spatial neglect. Cortex, 44, 68 – 78.

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Chapter 21

BIOGRAPHICAL SKETCH Keith R. Laws Title: Professor, University of Hertfordshire

EDUCATION

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Institution and Location University of Cambridge, UK

Degree

Year Conferred

Scientific Field

PhD

Contact points Address: School of Psychology University of Hertfordshire Hatfield Campus Hatfield AL10 9AB, UK

Professional Appointments Professor of Cognitive Neuropsychology

Honors C.Psychol, AFBPsS, FHEA

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Publications during last three years

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Book Laws, KR, Adlington R.L., Moreno-Martínez F.J. and Gale, T.M. Category-specificity: Evidence for Modularity of Mind. Nova. Published in January 2011 Published papers Moreno-Martinez FJ, Montoro PR, Laws KR. (2011). A set of high quality colour images with Spanish norms for seven relevant psycholinguistic variables: The Nombela naming test. Aging Neuropsychology and Cognition, 18, 293-327. Laws, KR, Kondel TK, Clarke R, and Nillo AM (2011). Delusion prone individuals: stuck in their ways? Psychiatry Research, 186, 219-224 Tyson, P.J., Wilson, K., Brailsford, R. and Laws, KR. Physical Activity and Mental Health in a student population (2010) Journal of Mental Health, 19, 492-499 Patel DD, Laws, KR, Padhi A, Farrow JM, Mukhopadhaya K, Krishnaiah R and Fineberg NA. (2010). The neuropsychology of the schizo-obsessive subtype of schizophrenia: a new analysis. Psychological Medicine, 40, 921-933 Pomarol-Clotet E, Haynes F, Ashwin C, Bullmore, ET., McKenna, P. J. and Laws, KR. (2010). Facial emotion processing in schizophrenia: a non-specific neuropsychological deficit. Psychological Medicine, 40, 911-919 Lynch, D., Laws, KR, and McKenna, P.J. (2010). Cognitive Behavioural Therapy for major psychiatric disorder: does it really work? A meta-analytical review of well-controlled studies. Psychological Medicine, 40, 9-24 Bhatt R, Laws, KR and McKenna PJ (2010). False memory in schizophrenia patients with and without delusions. Psychiatry Research, 178, 260-265 Laws, KR, Duncan, A and Gale, T.M (2010). ‗Normal‘ semantic-phonemic fluency discrepancy in Alzheimer's disease? A meta-analytic study. Cortex, 46, 595-601 Adlington R.L, Laws, KR, and Gale, T.M (2009). Visual processing in Alzheimer's disease: Surface detail and colour fail to aid object identification. Neuropsychologia, 47, 25742583 Adlington R.L, Laws, KR, and Gale, T.M (2009). The Hatfield Image Test (HIT): A new picture test and norms for experimental and clinical use. Journal of Clinical and Experimental Neuropsychology, 31, 731-753 Gale, T.M., Irvine, K., Laws, KR and Ferresy, S. (2009). The naming profile in Alzheimer patients parallels that of elderly controls. Journal of Clinical and Experimental Neuropsychology, 31, 565-574 Dibben, C.R.M., Rice C., Laws, KR, and McKenna P.J. (2009). Is executive impairment associated with schizophrenic syndromes? A meta-analysis. Psychological Medicine, 39, 381-392 Laws, KR, Gale, T.M., Moreno-Martínez F.J., Adlington R.L, Irvine K and Sthanakiya S. (2008). Category-specific Semantics in Alzheimer's Dementia and Normal Aging?; In Cognitive Psychology Research Developments (Ed:) Stella P. Weingarten and Helena O. Penat

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McKenna, P.J., Salvador, R., Lynch, D., Laws, KR (2008) Risk of harm after psychological intervention British Journal of Psychiatry 193 344-345 Moreno-Martínez, F.J., Laws, KR and Schulz J (2008). The impact of dementia, age and sex on category fluency: greater deficits in women with Alzheimer‘s disease. Cortex, 44, 1256-1264 Moreno-Martínez, F.J., Laws, KR and Goñi-Imízcoz, M. (2008). The Longitudinal Neurodegenerative Impact of Alzheimer‘s Disease on Picture Naming. In Alzheimer's Disease in the Middle-Aged (Ed: HS Jeong) Moreno-Martínez F.J., and Laws, KR (2008). No category specificity in Alzheimer‘s disease: a normal aging effect. Neuropsychology, 22, 485-490 Pomarol Clotet E., Oh, T, Laws, KR, and McKenna PJ (2008). Semantic Priming in Schizophrenia: Systematic Review and Meta-Analysis. British Journal of Psychiatry, 192, 92-97 Laws, KR., Patel, D.D., and Tyson, P.J. (2008). Awareness of everyday executive difficulties precede overt executive dysfunction in schizotypal subjects. Psychiatry Research, 160, 814

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Chapter 22

BIOGRAPHICAL SKETCH Iscia Lopes-Cendes Title: M.D., Ph.D. Department of Medical Genetics, Faculty of Medical Sciences, University of Campinas-UNICAMP, Campinas, SP, BRAZIL

Date of Birth: 04/04/1964

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EDUCATION Institution and Location

Degree

University of Campinas UNICAMP, Campinas, BRAZIL McGill University, Montreal, Canada.

M.D. degree Ph.D.

Year Conferred

Scientific Field

Neuroscience

Contact points Address: Tessalia Vieira de Camargo, 126. Cidade Universitária "Zeferino Vaz," Campinas, SP, 13083-887 Brazil

RESEARCH AND PROFESSIONAL EXPERIENCE I have experience in the filed of neurogenetics, treating patients with neurodegenerative disorders, as well as doing research in molecular genetics.

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Professional Appointments Professor of Medical Genetics and head of the Department of Medical Genetics, Faculty of Medical Sciences, University of Campinas-UNICAMP, Campinas, SP, Brazil

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Publications during last three years 1. Longitudinal MRI volumetric evaluation in patients with familial mesial temporal lobe epilepsy. Conz L, Morita ME, Coan AC, Kobayashi E, Yasuda CL, Pereira AR, LopesCendes I, Cendes F. Front Neurol. 2011 Feb 14;2:5. 2. MRI-Texture Analysis of Corpus Callosum, Thalamus, Putamen, and Caudate in MachadoJoseph Disease. De Oliveira MS, D'Abreu A, França Jr MC, Lopes-Cendes I, Cendes F, Castellano G. J Neuroimaging. 2010 Dec 1. doi: 10.1111/j.1552-6569.2010.00553.x. [Epub ahead of print] 3. Antiepileptic drug response in temporal lobe epilepsy: a clinical and MRI morphometry study. Bilevicius E, Yasuda CL, Silva MS, Guerreiro CA, Lopes-Cendes I, Cendes F. Neurology. 2010 Nov 9;75(19):1695-701. 4. MicroRNAs: a new paradigm on molecular urological oncology. Reis LO, Pereira TC, Lopes-Cendes I, Ferreira U. Urology. 2010 Sep;76(3):521-7. Epub 2010 May 15. Review. 5. Investigation of the 22q11.2 candidate region in patients with midline facial defects with hypertelorism. Simioni M, Freitas EL, Vieira TP, Lopes-Cendes I, Gil-da-Silva-Lopes VL. J Appl Genet. 2010;51(2):219-21. 6. Family-based association study for bipolar affective disorder. Secolin R, Banzato CE, Oliveira MC, Bittar MF, Santos ML, Dalgalarrondo P, Lopes-Cendes I. Psychiatr Genet. 2010 Jun;20(3):126-9. 7. Segregation analysis in mesial temporal lobe epilepsy with hippocampal atrophy. Secolin R, Maurer-Morelli C, Cendes F, Lopes-Cendes I. Epilepsia. 2010 Feb;51 Suppl 1:47-50. No abstract available. 8. Relationship between environmental factors and gray matter atrophy in refractory MTLE. Yasuda CL, Morita ME, Alessio A, Pereira AR, Balthazar ML, Saúde AV, Costa AL, Costa AL, Cardoso TA, Betting LE, Guerreiro CA, Damasceno BP, Lopes-Cendes I, Tedeschi H, de Oliveira E, Cendes F. Neurology. 2010 Mar 30;74(13):1062-8. 9. Thalamic volume and dystonia in machado-joseph disease. D'Abreu A, França MC Jr, Yasuda CL, Souza MS, Lopes-Cendes I, Cendes F. J Neuroimaging. 2011 Apr;21(2):e913. doi: 10.1111/j.1552-6569.2010.00464.x. 10. Genetic testing in the epilepsies--report of the ILAE Genetics Commission. Ottman R, Hirose S, Jain S, Lerche H, Lopes-Cendes I, Noebels JL, Serratosa J, Zara F, Scheffer IE. Epilepsia. 2010 Apr;51(4):655-70. Epub 2010 Jan 19. 11. Correlation between quantitative EEG and MRI in idiopathic generalized epilepsy. Betting LE, Li LM, Lopes-Cendes I, Guerreiro MM, Guerreiro CA, Cendes F. Hum Brain Mapp. 2010 Sep;31(9):1327-38. 12. Clinical correlates of autonomic dysfunction in patients with Machado-Joseph disease. França MC Jr, D'Abreu A, Nucci A, Lopes-Cendes I. Acta Neurol Scand. 2010 Jun;121(6):422-5. Epub 2010 Jan 11.

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13. MEF2C silencing attenuates load-induced left ventricular hypertrophy by modulating mTOR/S6K pathway in mice. Pereira AH, Clemente CF, Cardoso AC, Theizen TH, Rocco SA, Judice CC, Guido MC, Pascoal VD, Lopes-Cendes I, Souza JR, Franchini KG. PLoS One. 2009 Dec 29;4(12):e8472. 14. Caring for Machado-Joseph disease: current understanding and how to help patients. D'Abreu A, França MC Jr, Paulson HL, Lopes-Cendes I. Parkinsonism Relat Disord. 2010 Jan;16(1):2-7. Epub 2009 Oct 6. Review. 15. Prospective study of peripheral neuropathy in Machado-Joseph disease. C França M Jr, D'abreu A, Nucci A, Cendes F, Lopes-Cendes I. Muscle Nerve. 2009 Dec;40(6):1012-8. 16. Cryptic anhydrobiotic potential in man: implications in medicine. Pereira TC, LopesCendes I. Med Hypotheses. 2009 Oct;73(4):506-7. Epub 2009 Jul 14. 17. Progression of ataxia in patients with Machado-Joseph disease. França MC Jr, D'Abreu A, Nucci A, Cendes F, Lopes-Cendes I. Mov Disord. 2009 Jul 15;24(9):1387-90. 18. A combined voxel-based morphometry and 1H-MRS study in patients with Friedreich's ataxia. França MC Jr, D'Abreu A, Yasuda CL, Bonadia LC, Santos da Silva M, Nucci A, Lopes-Cendes I, Cendes F. J Neurol. 2009 Jul;256(7):1114-20. Epub 2009 Mar 12. 19. Experimental animal model and RNA interference: a promising association for bladder cancer research. Reis LO, Pereira TC, Favaro WJ, Cagnon VH, Lopes-Cendes I, Ferreira U. 20. Expression profile and distribution of Efhc1 gene transcript during rodent brain development. Conte FF, Ribeiro PA, Marchesini RB, Pascoal VD, Silva JM, Oliveira AR, Gilioli R, Sbragia L, Bittencourt JC, Lopes-Cendes I. J Mol Neurosci. 2009 Sep;39(1-2):69-77. Epub 2009 Feb 4. 21. Sleep symptoms and their clinical correlates in Machado-Joseph disease. D'Abreu A, França M Jr, Conz L, Friedman JH, Nucci AM, Cendes F, Lopes-Cendes I. Acta Neurol Scand. 2009 Apr;119(4):277-80. Epub 2008 Sep 3.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 23

BIOGRAPHICAL SKETCH Paul R. Martin Title: Griffith University

Date of Birth: 22nd February, 1951

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EDUCATION Institution and Location

Degree

University of Bristol, UK.

Bachelor of Science (Honours).

Diploma in Clinical Psychology. British Psychological Society, UK. University of Oxford, UK.

Year Conferred 1968-1972

Scientific Field

1972-1977

1972-1977

Doctor of Philosophy.

Contact points Address: School of Psychology Griffith University, Mount Gravatt Campus 176 Messines Ridges Road Mount Gravatt, Qld 4122 Australia

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RESEARCH AND PROFESSIONAL EXPERIENCE Paul Martin‘s publication record includes: 8 authored and edited books; 129 chapters, articles and research reports; and 114 conference presentations. He is the primary author on 80% of these publications. His journal publications include articles in first-rank international journals in health psychology (Health Psychology, Psychology and Health, British Journal of Health Psychology), behaviour therapy (Behavior Therapy, Behaviour Research and Therapy, Journal of Behavioral Medicine), clinical psychology (Clinical Psychology Review, British Journal of Clinical Psychology) and psychosomatic medicine (Journal of Psychosomatic Research), in addition to the leading specialist journals in my main research field, Cephalalgia (impact factor of 3.464) and Headache (impact factor of 2.786). His books have been published by major international publishers including Pergamon, Guilford, John Wiley, Macmillan, Academic, and Wiley-Blackwell. He has given 21 Keynote Addresses across several countries including Australia, UK, Germany, Italy, USA, South Africa and Thailand. Current invitations reflect the breadth of his interests as they include: a Keynote Address on the future of clinical psychology at the APS National Clinical Psychology Conference (Sunshine Coast, July, 2011); an Invited Symposium on translating science into practice at the American Psychological Association Convention (Washington, USA, August, 2011); and a Keynote Address on his headache research at the 30th International Congress of Psychology (Cape Town, South Africa, July, 2012). He has given 21 Invited Workshops across several countries including Australia, USA, Canada, Denmark, Italy and Thailand.

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Professional Appointments National President of the Australian Behaviour Modification Association (1984-1985). Chair, 30th Annual Conference, Australian Psychological Society (1994-1995). Director of Science, Australian Psychological Society (1997-2000). President, Australian Psychological Society (2000-2004). President, 27th International Congress of Applied Psychology (2003-2010).

Honors 1993 Fellow, Australian Psychological Society. 2007 Fellow, British Psychological Society. 2007 Honorary Fellow, Australian Psychological Society. The Constitution of the APS limits the number of Honorary Fellows to 15 in a Society with almost 19,000 members (currently there are 10). 2010 Fellow, International Association of Applied Psychology. 2003 Centenary Medal, General List. Commemorative Medal awarded by the Commonwealth Government for services to Australian society and medicine. 2011 Citation for Excellence, American Psychological Association (to be presented at the APA Convention in Washington in August, 2011).

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Publications during last three years Martin, P.R., Cheung, F., Knowles, M., Kyrios, M., Littlefield, L., Overmier, B., & Prieto, J.M. (Eds.). (2011). The IAAP handbook of applied psychology. Oxford: WileyBlackwell. Martin, P.R. (2009). Psychological management. In P. Selvaratnam, K. Niere & M. Zuluaga (Eds.), Headache, orofacial pain and bruxism (pp.277-288). Edinburgh, UK: Churchill Livingstone Elsevier. Martin, P.R. (2011). Applied psychology in the international context: What more needs to be done? In P.R. Martin, F. Cheung, M. Knowles, M. Kyrios, L. Littlefield, B. Overmier, & J.M. Prieto, (Eds.). The IAAP handbook of applied psychology. Oxford: Wiley-Blackwell. Ugalde, A., Martin, P.R., & Rees, G. (2008). Psychological impact of receiving genetic risk information for breast cancer, with and without lifestyle information. Australian Journal of Psychology, 60, 1-9. Rees, G., Martin, P.R. & Macrae, F.A. (2008). Screening participation in individuals with a family history of colorectal cancer: A review. European Journal of Cancer Care, 17, 221-232. Martin, P.R., & MacLeod, C. (2009). Behavioral management of headache triggers: Avoidance of triggers is an inadequate strategy. Clinical Psychology Review, 29, 483495. Martin, P.R. (2010). Managing headache triggers: Think ―coping‖ not ―avoidance‖. Cephalalgia, 30, 634-637. Martin P.R. (2010). Behavioral management of migraine headache triggers: Learning to cope with triggers. Current Pain and Headache Reports, 14, 221-227. Martin, P.R. (2010). Migraine: Consider referring to a psychologist. Pain Management in General Practice, 1, 12-15. Martin, P.R., Reece, J.R., Lauder, S., & McClelland, A. (in press). A randomized control trial of a social support intervention. Health Psychology: Health and Well-Being.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 24

BIOGRAPHICAL SKETCH Martin H. Maurer Title: University of Heidelberg, Germany

Date of Birth: Dec. 16, 1971

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EDUCATION Institution and Location

Degree

Medical Faculty, University of Heidelberg, Germany, 1999

M.D.

Year Conferred 1992-99

Scientific Field

Contact points Address: Dept. of Physiology and Pathophysiology, University of Heidelberg, Im Neuenheimer Feld 326, 69120 Heidelberg, Germany. Present address: Mariaberg Hospital for Child and Adolescent Psychiatry, Burghaldenstr. 12, 72501 Gammertingen-Mariaberg, Germany. Email: [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE 2000-2005 Post-doctoral Fellow, Dept. of Physiology and Pathophysiology, University of Heidelberg, 2003 Post-doctoral Fellow, Dept. of Psychiatry and Behavioral Sciences, The Johns Hopkins University, Baltimore, Md., U.S.A., 2008-2009 Research group leader, SYGNIS Bioscience GmbH & Co. KG, 2009-2010 Resident in Pediatrics, Stuttgart, Germany, 2011-present, Resident in Child and Adolescent Psychiatry, Mariaberg Hospital

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Professional Appointments 2005 Assistant Professor, 2007 Associate Professor, University of Heidelberg

Honors Editorial Board Member: The Application of Clinical Genetics, The American Journal of Stem Cells, Stem Cell Research and Therapy, The Open Enzyme Inhibition Journal.

Publications during last three years

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Journal articles Maurer MH. Proteomic definitions of mesenchymal stem cells. Stem Cells Int. 2011 Mar 3;2011:704256. PubMed PMID: 21437194; PubMed Central PMCID: PMC3062154. Wohnsland S, Bürgers HF, Kuschinsky W, Maurer MH. Neurons and neuronal stem cells survive in glucose-free lactate and in high glucose cell culture medium during normoxia and anoxia. Neurochem Res. 2010 Oct;35(10):1635-42. Epub 2010 Jul 3. PubMed PMID: 20602256. Kalenka A, Gross B, Maurer MH, Thierse HJ, Feldmann RE Jr. Isoflurane anesthesia elicits protein pattern changes in rat hippocampus. J Neurosurg Anesthesiol. 2010 Apr;22(2):144-54. PubMed PMID: 20118798. Maurer MH. Proteomics of brain extracellular fluid (ECF) and cerebrospinal fluid (CSF). Mass Spectrom Rev. 2010 Jan-Feb;29(1):17-28. Review. PubMed PMID: 19116946. Schordan S, Schordan E, Endlich N, Lindenmeyer MT, Meyer-Schwesinger C, Meyer TN, Giebel J, Cohen CD, Endlich K, Maurer MH. Alterations of the podocyte proteome in response to high glucose concentrations. Proteomics. 2009 Oct;9(19):4519-28. PubMed PMID: 19688724. Canis M, Mack B, Gires O, Maurer MH, Kuschinsky W, Duembgen L, Duelli R. Increased densities of monocarboxylate transport protein MCT1 after chronic administration of nicotine in rat brain. Neurosci Res. 2009 Aug;64(4):429-35. Epub 2009 May 9. PubMed PMID: 19433117. Hinkelbein J, Feldmann RE Jr, Schubert C, Peterka A, Schelshorn D, Maurer MH, Kalenka A. Alterations in rat serum proteome and metabolome as putative disease markers in sepsis. J Trauma. 2009 Apr;66(4):1065-75. PubMed PMID: 19359916. Schelshorn DW, Schneider A, Kuschinsky W, Weber D, Krüger C, Dittgen T, Bürgers HF, Sabouri F, Gassler N, Bach A, Maurer MH. Expression of hemoglobin in rodent neurons. J Cereb Blood Flow Metab. 2009 Mar;29(3):585-95. Epub 2008 Dec 31. PubMed PMID: 19116637. Canis M, Maurer MH, Kuschinsky W, Duembgen L, Duelli R. Increased densities of monocarboxylate transporter MCT1 after chronic hyperglycemia in rat brain. Brain Res. 2009 Feb 27;1257:32-9. Epub 2008 Dec 11. PubMed PMID: 19118535.

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Berger C, Xia F, Maurer MH, Schwab S. Neuroprotection by pravastatin in acute ischemic stroke in rats. Brain Res Rev. 2008 Jun;58(1):48-56. Epub 2007 Nov 1. Review. PubMed PMID: 18035423. Bürgers HF, Schelshorn DW, Wagner W, Kuschinsky W, Maurer MH. Acute anoxia stimulates proliferation in adult neural stem cells from the rat brain. Exp Brain Res. 2008 Jun;188(1):33-43. Epub 2008 Mar 11. PubMed PMID: 18330547. Maurer MH, Haux D, Unterberg AW, Sakowitz OW. Proteomics of human cerebral microdialysate: From detection of biomarkers to clinical application. Proteomics Clin Appl. 2008 Mar;2(3):437-43. doi: 10.1002/prca.200780044. Epub 2008 Feb 13. PubMed PMID: 21136845. Maurer MH, Feldmann RE Jr, Bürgers HF, Kuschinsky W. Protein expression differs between neural progenitor cells from the adult rat brain subventricular zone and olfactory bulb. BMC Neurosci. 2008 Jan 16;9:7. PubMed PMID: 18197988; PubMed Central PMCID: PMC2244614. Maurer MH, Schäbitz WR, Schneider A. Old friends in new constellations—the hematopoetic growth factors G-CSF, GM-CSF, and EPO for the treatment of neurological diseases. Curr Med Chem. 2008;15(14):1407-11. Review. PubMed PMID: 18537618. Feldmann RE Jr, Maurer MH, Hunzinger C, Lewicka S, Buergers HF, Kalenka A, Hinkelbein J, Broemme JO, Seidler GH, Martin E, Plaschke K. Reduction in rat phosphatidylethanolamine binding protein-1 (PEBP1) after chronic corticosterone treatment may be paralleled by cognitive impairment: a first study. Stress. 2008;11(2):134-47. PubMed PMID: 18311602.

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Books and book chapters Maurer MH (ed.) (2012) Amyotrophic Lateral Sclerosis. InTech, Rijeka. Maurer MH (2012) Two-Dimensional Protein Analysis of Neural Stem Cells. In: Karamanos Y (ed.), Expression Profiling in Neuroscience (Neuromethods, vol. 64), Humana / Springer, Totowa, N.J. Maurer MH (2011) Muskelphysiologie. In: Jäger J, Krüger K (eds.) Der Muskel im Sport. KVM, Marburg. Maurer MH (2008) Physiologiekarten. KVM, Marburg.

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Chapter 25

BIOGRAPHICAL SKETCH Eiji Nakagawa Title: PhD, M.D. Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry

Date of Birth: 15 January, 1960

EDUCATION

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Institution and Location School of Medicine, University of Tsukuba

Degree

Year Conferred

Scientific Field

Contact points Address: 4-1-1, Ogawahigashi-cho, Kodaira, Tokyo 187 8551, Japan

Professional Appointments Chief of Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry Visiting Professor, Department of Education, Faculty of Liberal Arts, Teikyo University

Publications during last three years 33 paper

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Chapter 26

BIOGRAPHICAL SKETCH Takehiko Nakama Title: Ph.D.

Date of Birth: October 13, 1970

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EDUCATION Institution and Location

Degree

The Johns Hopkins University in Baltimore The Johns Hopkins University in Baltimore The Johns Hopkins University in Baltimore

Ph.D.

Year Conferred August 2009

Ph.D.

August 2003

NIMH doctoral training program

May 2003

The Johns Hopkins University in Baltimore

Master of Science

May 2003

Scientific Field Applied Mathematics and Statistics Psychological and Brain Sciences Perceptual and Cognitive Neuroscience Engineering

Contact points European Center for Soft Computing Edificio Científico-Tecnológico C/ Gonzalo Gutiérrez Quirós, s/n 33600 Mieres, Spain Phone: +34 985 456 545 Fax: +34 985 456 699

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Department of Applied Mathematics and Statistics The Johns Hopkins University 3400 N. Charles Street Baltimore, MD 21218 USA Phone: +1 410-516-7198 Fax: +1 410-516-7459

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RESEARCH AND PROFESSIONAL EXPERIENCE European Center for Soft Computing, Mieres, Spain, October 2009-present Conducting research in soft computing with Enrique Ruspini, Enric Trillas, and Ana Colubi. Department of Applied Mathematics and Statistics, Johns Hopkins University, Baltimore, Maryland, January 2004-August 2009 Conducted dissertation research in probability with James Allen Fill. Kennedy Krieger Institute, Johns Hopkins University, Baltimore, Maryland, AugustSeptember 2008 Assisted statistical analysis to examine how parents with autistic children cope with emotional stress. Johns Hopkins University School of Medicine, Baltimore, Maryland, August-October 2005 Assisted statistical analysis to identify behavioral prototypes of children with attention deficit hyperactivity disorder. Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland, June 1998August 2003 Conducted dissertation research in single-unit neurophysiology. National Institute of Bioscience and Human Technology, Tsukuba, Ibaraki, Japan, June 1995May 1996 Conducted research on the effects of background familiarity in visual search.

Professional Appointments Postdoctoral research fellow, European Center for Soft Computing

Honors Award for Excellence in Teaching, Department of Applied Mathematics and Statistics, 2009 Best Paper Award, 2008 International Symposium on Neural Networks Best Paper Award, 2008 ACIS International Conference on Software Engineering, Artificial Intelligence, Networking, and Parallel/Distributed Computing George M.L. Sommerman Engineering Graduate Teaching Assistant Award, 2006 (a university-wide award) Award for Excellence in Teaching, Department of Applied Mathematics and Statistics, 2004 AT&T Asia/Pacific Leadership Award, 1996

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Summa Cum Laude (highest distinction), State University of New York College at Oswego, 1995 President's List for the Spring 1995 semester, State University of New York College at Oswego President's List for the Fall 1994 semester, State University of New York College at Oswego

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Publications during last three years Nakama, T. (2010). Markov chain analysis of genetic algorithms applied to fitness functions perturbed concurrently by additive and multiplicative noise. To appear in Computational Optimization and Applications. Nakama, T., Colubi, A. & Lubiano, M. A. (2010). Two-way analysis of variance for intervalvalued Data. In: Borgelt, C. et al., eds. Combining Soft Computing and Statistical Methods in Data Analysis, 77, 475-482, Springer-Verlag, Berlin. Fill, J.A., & Nakama, T. (2010). Analysis of the expected number of bit comparisons required by Quickselect. Algorithmica, 58, 730-769. Trillas, E., Nakama, T., & García-Honrado, I. (2010). Fuzzy Probabilities: Tentative Discussions on the Mathematical Concepts. Proceedings of the International Conference on Information Processing and Management of Uncertainty in Knowledge-Based Systems, 139-148. Nakama, T. (2009). Theoretical analysis of batch and on-line training for gradient descent learning in neural networks. Neurocomputing, 73, 151-159. (This paper was selected as one of the best papers of 2008 International Symposium on Neural Networks.) Nakama, T. (2009). Convergence properties of genetic algorithms in a wide variety of noisy environments. CMC: Computers, Materials, & Continua, 14, 35-60. Nakama, T. (2009). Using genetic algorithms to find a globally optimal solution in uncertain environments with multiple sources of noise. Proceedings of the International Conference on Computational and Experimental Engineering and Sciences, 113-122. Nakama, T. (2009). A Markov chain that models genetic algorithms in noisy environments. To appear in Nonlinear Analysis Series A: Theory, Methods \& Applications. Nakama, T. (2009). Markov chain analysis of genetic algorithms in a wide variety of noisy environments. Proceedings of the 2009 Genetic and Evolutionary Computation Conference, 827-834. Nakama, T. (2009). Transition and convergence properties of genetic algorithms applied to fitness functions perturbed concurrently by additive and multiplicative noise. Proceedings of IEEE Congress on Evolutionary Computation, 2662-2669. Nakama, T. (2008). Markov chain analysis of genetic algorithms applied to fitness functions perturbed by multiple sources of additive noise. Studies in Computational Intelligence, 149, 123-136. (This paper was selected as one of the 19 best papers of 2008 ACIS International Conference on Software Engineering, Artificial Intelligence, Networking, and Parallel/Distributed Computing.)

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Nakama, T. (2008). Theoretical analysis of genetic algorithms in noisy environments based on a Markov model. Proceedings of the 2008 Genetic and Evolutionary Computation Conference, 1001-1008. Nakama, T. (2008). Markov chain analysis of genetic algorithms in a noisy environment. Proceedings of the 2008 International Conference on Engineering Optimization, Evolutionary Techniques, Paper Code 516, 1-10. Fill, J.A., & Nakama, T. (2008). Analysis of the expected number of bit comparisons required by Quickselect. Proceedings of the Fourth Workshop on Analytic Algorithmics and Combinatorics, 249-256.

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Chapter 27

BIOGRAPHICAL SKETCH J. Patrick Neary Title: Dr. Faculty of Kinesiology & Health Studies, University of Regina

Date of Birth: May 26, 1957

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EDUCATION Institution and Location

Degree

University of Victoria, BC, Canada University of Victoria, BC, Canada University of Alberta

BEd MA PhD

Year Conferred

Scientific Field

Contact points Address: CK 164.23, University of Regina, 3737 Wascana Parkway, Regina, SK, S4S 0A2

RESEARCH AND PROFESSIONAL EXPERIENCE 20 years teaching and research experience

Professional Appointments Full Professor, University of Regina; Executive Director, Dr. Paul Schwann Applied Health & Research Centre; Research Associate, Regina Qu'Appelle Health Region

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Honors Career Achievement Award, University of Regina (2009) Promotion to Full Professor (July 2008) Special Merit Award, University of Regina (2007) Special Merit Award, University of Regina (2006) Special Merit Award, University of New Brunswick (2004-2005) Nominated for the Allan P. Stuart Teaching Award, University of New Brunswick (April 2004) Canadian Association of Sport Sciences Young Investigator Award (October 1991)

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Publications Last 3 Years Salmon, D.M., Harrison, M.F., Neary, J.P. (2011). "Neck Pain in Military Helicopter Aircrew and the Role of Exercise Therapy. Aviat Space Environ Med, Accepted In Press. Harrison, M.F., J.P. Neary, W.J. Albert, V.L. Chester, J.C. Croll, V.C Chancey, B.A. Bumgardner. (2010). Differentiation of physiologic measures of neck myalgia using principal components analysis. J Electromyogr Kinesiol, Accepted In Press. Len, T.K., Neary, J.P., Asmundson, G.J.G., Goodman, D., Bjornson, B., Bhambani, Y.N. (2010). Analysis of cerebrovascular responses following mild traumatic brain injury. Med Sci Sports Exerc, Submitted in Press Len, T.K., Neary, J.P. (2011). Cerebrovascular pathophysiology following mild traumatic brain injury. Clin Physiol Funct Image, 31:85-93. Forde, K.A., Albert, W.J., Harrison, M,F., J.P. Neary, Croll, J.C., Callaghan, J.P. (2011) Neck loads and postures experienced by Canadian Forces helicopter pilots during simulated day and night flights. Int J Ind Erg 41(2): 128-135. Harrison M.F., Neary, J.P., Albert, W.J., McKenzie, N.P., Veillette, D.W., Croll, J.C. (2010). Cytochrome oxidase changes trapezius muscles with night vision goggle usage. Int J Ind Erg 40:140-145 (Special Issue, Invited Submission) (DND). Harrison, M.F., Neary, J.P., Albert, W.J., Kuruganti, U., Croll, J., Chancey, V.C., Bumgardner, B.A. (2009) Measuring neuromuscular fatigue in cervical spinal musculature of military helicopter aircrew. Mil Med. 174:1183-9. Morrison, SA, Slievert, G.G., Neary, J.P., Cheung, S.S. (2009). Prefrontal cortex oxygenation is preserved and does not contribute to impaired neuromuscular activation during passive hyperthermia. Appl Physiol Nutr Metab. 34:66-74 (NSERC). Neary, J.P., Roberts, A., Leavins, N., Harrison, M.F., Croll, J.C., Sexsmith, J.R.(2008). Prefrontal lobe oxygenation during incremental exercise in chronic fatigue syndrome. Clin Physiol Funct Image 28:364-372 (NSERC).

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 28

BIOGRAPHICAL SKETCH Kirill Nikolayevich Dudkin Title: Pavlov Institute of Physiology of Russian Acad. of Sciences

Date of Birth: July 7, 1936

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EDUCATION Institution and Location

Degree

Scientific Field

B.S.

Year Conferred 1967

from Leningrad Politechnic Institute, Russia Pavlov Institute of Physiolgy of Russian Acad. of Sciences, Russia Pavlov Institute of Physiolgy of Russian Acad. of Sciences, Russia

Ph. D.

1971

Biophysics

Dr.

1988

Biol. Sci. (Neuroscience)

Contact points Address: 199034 Russia, Sankt-Petersburg, nab. Makarova, 6

RESEARCH AND PROFESSIONAL EXPERIENCE Neuropsychological and psychophysiological approaches to visual and cognitive information processing; behavioral studies on monkeys; multichannel recording and analysis of single units activity in brain of animal (cat and monkey); pharmacological testing and microdialysis technique; neurochemical mechanisms of behavior; automatic control and computing technique in physiological experiments; neural models of information processing.

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Professional Appointments 1962 - 1971 - Senior Engineer of Visual Physiology lab. of I.P. Pavlov Institute of Physiology, Russian Acad. Sci. 1971 - 1986 - Junior Research Associate in Pavlov Institute of Physiology. 1986 - 1989 - Senior Research Associate in Pavlov Institute of Physiology. 1989 - 1997 - Leading Research Associate in Laboratory of Regulation of Neuronal Functions in Pavlov Institute of Physiology, Russian Academy of Sciences. 1997 - up to now - Head of Department of bioinformatics and modeling of physiological functions, Pavlov Institute of Physiology of the Russian Academy of Sciences

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Publications during last three years Dudkin K.N., Chueva I.V. Cognitive structures in conditioned reflex behavior in monkeys: dependence on the type of sensory information. Russian J. of Physiology. 2008. 94(1): P. 81- 94. Dudkin K.N., Chueva I.V., Makarov F.N. Invariant visual-recognition learning in monkey: Effect of hemispheric specialization of the prefrontal cortex. International Journal of Psychophysiology. 2008. 69(3): 140. Dudkin K.N., Chueva I.V., Makarov F.N. Interaction of sensory and cognitive processes in monkeys in the conditioned reflex behavior: the role of cholinergic and glutamatergic mechanisms of the cortex. In: Neurochemical mechanisms of the adaptive and pathological brain states. Sankt-Petersburg. 2008. P. 49 – 50. Dudkin K.N., Chueva I.V. Formation of cognitive: structures in conditioned reflex behavior in monkeys relationship with type of vision information. Neurosci. Behav. Physiol. 2009. 39(2):183-191 Dudkin K.N. Organization of the conditioned reflex behavior as the result of the interaction of sensory, cognitive, and control (attention and motivation) processes. Robotics. Looking into the future. 2010. P. 56 - 59.. Dudkin K.N.,Mironov S.V., Vaido A.I.., Makarov F.N. Specialized informational systems for image analysis in physiological studies. Russian J. of Physiology. 2010. 96(3): 325-334. Dudkin K.N., Chueva I.V., Makarov F.N. Neurophysiologic basis of cognitive function: the role of hemispheric asymmetry of prefrontal and parietal cortex. 4th International Conference on Cognitive Science. 2010. V.1.P. 251 - 253. Dudkin K.N., Chueva I.V. Neuroinformatics principles of behavior organization. In: Hi-Tech. International Conf. Sankt-Petersburg. 2011. P. 199-206.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 29

BIOGRAPHICAL SKETCH Alan M. Palmer Title: Professor

Date of Birth: 4 January 1958

EDUCATION Degree: BSc; MSc; PhD

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Contact points [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE 2008-present: MS Therapeutics Ltd*; Director and Chief Scientific Officer 2003- present: School of Pharmacy; Visiting Professor; 2002- 2006: Pharmidex Pharmaceutical Services*; Chief Executive Officer 1999-2002: Vernalis Research Limited; Distinguished Research Fellow 1998-2002: Cerexus Ltd*; Board Director 1995-1999: Cerebrus Ltd*; Director of Neurochemistry 1994-1995: Wyeth Research (U.K.); Principal Research Scientist 1989-1994: Dept. of Psychiatry; Assistant Professor; University of Pittsburgh 1990-1994: Dept. of Pharmacology; Assistant Professor; University of Pittsburgh 1984-1989: Institute of Neurology; Miriam Marks Research Fellow 1981-1984: Institute of Neurology; Research Assistant *Founder

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Professional Appointments Fellow of the Society of Biology, Director of One Nucleus, Scientific a member of the Scientific Advisory Board of GE Healthcare Medical Diagnostics, Chairman of the Society for Medicines Research.

Honors Voted 'Entrepreneur of the Year' by the London Biotechnology Network in 2005

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Publications Last 3 Years Palmer A.M, Stephenson J.A., Willliams R.J. (2007) Society for Medicines Research: 40th Anniversary Symposium Drug News and Perspectives, 20(3):191-196. Palmer A.M, (2007) Drugs for dementia. Education in Chemistry, January Karran E and Palmer A.M, (2007) Neurodegenerative disorders and their treatment Drug News and Perspectives, 20(6):407-412. Cowley P., Palmer A.M, and Williams R (2008) Obesity and its treatment Drugs of the Future, 2008, 33: 1077-1082. Palmer AM (2008) Pharmacotherapy for obesity: progress and prospects, Drug Discovery Today, 3, 7, Alavijeh MS and Palmer A.M (2008) Pharmacotherapy for CNS disorders: Progress and prospects, Preclinical World, 33-37. Alavijeh MS and Palmer A.M (2008) CNS Disorders and their treatment, Preclinical World, 38- 39. Palmer AM (2009) Pharmacotherapy for multiple sclerosis. Curr Opin Investig Drugs. 10: 407-417. Palmer AM (2010) The blood-brain barrier. Neurobiol. Disease, 37: 1-2 Palmer AM (2010) The role of the blood-CNS barrier in CNS disorders and their treatment. Neurobiol. Disease 37:. 3-12 Alavijeh MS and Palmer A.M (2010) Measurement of the pharmacokinetics and pharmacodynamics of neuroactive compounds. Neurobiol. Disease, 37: 38-47. Ash ES, Alavijeh MS, Palmer AM, Mitchelmore C, Howlett DR, Francis PT, Broadstock M, Richardson JC. (2010) Neurochemical changes in a double transgenic mouse model of Alzheimer's disease fed a pro-oxidant diet. Neurochem Int.;57::504-511. Dixon J, England P, Lawton G, Machin P, Palmer A. (2010). Medicines discovery in the 21st century: the case for a stakeholder corporation. Drug Discov Today. 15::700-703. Palmer A.M. (2010) Teriflunomide, an inhibitor of dihydroorotate dehydrogenase for the potential oral treatment of multiple sclerosis. Curr Opin Investig Drugs 11:1313-1323.

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Chapter 30

BIOGRAPHICAL SKETCH José Miguel Pêgo Title: Life and Health Sciences Research Institute (ICVS), School of Health Sciences

Date of Birth: 31/10/1977

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EDUCATION Institution and Location

Degree

Year Conferred

University of Minho, Braga (Portugal), Ciências da Saúde - Ciências Biológicas e Biomédicas. University of Porto, Porto (Portugal), Medicine

PhD

01/2008

MD

07/2001

Scientific Field

Contact points Address:

RESEARCH AND PROFESSIONAL EXPERIENCE • • •

From 02/2008 to Present Day: ICVS/ECS - University of Minho (Braga, Portugal), investigator, neurosciences From 10/2003 to 01/2008: ICVS/ECS - University of Minho (Braga, Portugal), PhD Student, neurosciences From 10/2001 to 09/2003: ICVS/ECS - University of Minho (Braga, Portugal), trainee, neurosciences

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Professional Appointments Auxilliary Professor (Pharmacology) at School of Health Sciences – University of Minho Portugal Assistant Anesthesiologist at Centro Hospitalar do Alto Ave - Portugal

Honors Grünenthal Pain Prize 2003 Grünenthal Pain Prize 2007

Publications during last three years •





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Oliveira, M.; Leão, Pedro; Pêgo, José M; Cerqueira, João J; Rodrigues, Ana J. Sousa, Nuno 2011. "ProgrammingEffects of Antenatal Corticosteroids Exposure in Male Sexual Behavior.", The Journal of Sexual Medicine, 10000:10000 - 10001. Pêgo, José M; Sousa, Nuno; Sousa, João C; Almeida, Osborne F. X. 2010. Stress and the Neuroendocrinology ofAnxiety Disorders. In Behavioral Neurobiology of Anxiety and Its Treatment, ed. Stein, Murray B.; Steckler, Thomas, 97 - 120. ISBN: 978-3-642-02911-. Berlin Heidelber: Springer-Verlag. Bessa, João M; Mesquita, Ana R; Oliveira, Mário; Pêgo, José M; Cerqueira, João J; Palha, Joana A; Almeida,Osborne F. X; Sousa, Nuno. 2009. "A trans-dimensional approach to the behavioral aspects of depression", Frontiersin Behavioral Neuroscience 3, 1: 1 - 7. Rolanda, Carla; Lima, E.; Silva, D.; Moreira, I.; Pêgo, José M; Macedo, G.; CorreiaPinto, J.. 2009. "Invivoassessment of gastrotomy closure with over-the-scope clips in an experimental model for varicocelectomy (withvideo).",GastrointestEndosc 70, 6: 1137 - 1145. Pinto-Ribeiro, Filipa; Pêgo, José M; Sousa, Nuno; Leão, Pedro; Almeida, Armando. 2009. "Antinociception inducedby chronic glucocorticoid treatment is correlated to local modulation of spinal neurotransmitter content.", MolecularPain, 5: 41 - 52. Pêgo, José M; Salgado, António; Sousa, Nuno; Malva, João O; Sousa, R A; Fraga, Joana S; Silva, B A; Neves, N M;Reis, Rui L. 2009. "Effects of Starch/ Polycaprolactone-based Blends for Spinal Cord Injury Regeneration inNeurons/Glial Cells Viability and Proliferation ", Journal of Bioactive and Compatible Polymers 24, 3: 235 - 248. Gonçalves, Leonor; Silva, Rui; Pinto-Ribeiro, Filipa; Pêgo, José M; Bessa, João M; Pertovaara, Antti; Sousa, Nuno;Almeida, Armando. 2008. "Neuropathic pain is associated with depressive behaviour and induces neuroplasticity inthe amygdala of the rat", Experimental Neurology 213, 1: 48 - 56.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Research Biographies - José Miguel Pêgo •

Lima, Estevão; Rolanda, Carla; Osório, Luís; Pêgo, José M; Silva, David; HenriquesCoelho, Tiago; Carvalho, José L;Bergström, Maria; Park, Per-Ola; Mosse, Charles A; Swain, Paul; Correia-Pinto, Jorge. 2008. "Endoscopic Closure ofTransmural Bladder Wall Perforations", European Urology 178, 6: 2648 - 54. Pêgo, José M; Morgado, P; Pinto, L G; Cerqueira, João J; Almeida, Osborne F. X; Sousa, N. 2008. "Dissociation ofthe morphological correlates of stress-induced anxiety and fear", The European Journal of Neuroscience 27, 6: 1503 -16.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 31

BIOGRAPHICAL SKETCH Mauro Pessia Title: Section of Human Physiology, University of Perugia School of Medicine, Perugia, Italy

Date of Birth: April 20th, 1961

EDUCATION

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Institution and Location Diploma of Qualified Chemist, N. Parravano Chemistry Institute, Arpino (FR). Laurea in Pharmacy, University of Rome ―La Sapienza‖, Rome Diploma of Qualified Chemist, N. Parravano Chemistry Institute, Arpino (FR). Diploma of Specialist in Biomedical Research, ―Mario Negri Institute‖ CMNS, S. Maria Imbaro (Chieti)

Degree

Year Conferred 1980

Scientific Field

1986 1980 Ph.D.

1993

Contact points Address University of Perugia School of Medicine Department of Internal Medicine Section of Human Physiology Via del Giochetto I-06126 Perugia, ITALY

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Professional Appointments Research Assistant Professor 1995, Vollum Institute, Oregon Health Sciences University, Portland, OR, U.S.A. Group Leader 1996-1998, Laboratory of Potassium Channels Pathophysiology ―Mario Negri‖ Institute, CMNS, S. Maria Imbaro (Chieti) Italy. Unit Chief 1999-2002 Laboratory of Potassium Channels Pathophysiology, ―Mario Negri‖ Institute, CMNS, S. Maria Imbaro (Chieti) Italy. Associate Professor of Physiology, 2002- University of Perugia School of Medicine(Perugia) Italy.

Honors Alfredo Leonardi Prize for Rare Diseases., Awarded in 1998 to M.C. D'Adamo for her studies on Episodic Ataxia Type-1 carried out in my laboratory. Research grants awarded by Telethon Italy, by the National Research Council and by Compagnia di San Paolo.

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Publications during last three years 1. Sicca F., Imbrici P., D‘Adamo M.C., Moro F., Bonatti F., Brovedani P, Grottesi A., Guerrini R., Masi G., Santorelli F.M., and Pessia M. (2011). Gain-of-function of the Inwardly-Rectifying K+ Channel Kir4.1 in Autism with Seizures and Intellectual Disability. Neurobiology of Disease (in press). 2. Imbrici P., D‘Adamo M.C., Grottesi A., Biscarini A. and Pessia M. (2011). Episodic Ataxia Type 1 Mutations Affect Fast Inactivation of K+ Channels by a Reduction in Either Subunit Surface Expression or Affinity for Inactivation Domain Am. J. Physiol.Cell Physiology February 9 [Head of Print]. 3. D‘Adamo M. C., Shang L., Imbrici P; Brown S.D.M., Pessia M. @*, Tucker S.* (2011). Genetic inactivation of Kcnj16 identifies Kir5.1 as an important determinant of neuronal PCO2/pH sensitivity J. Biol. Chem. 286, 192-198 (published online 3 November 2010, 10.1074/jbc.M110.189290; @Corresponding author; *Autori che hanno contribuito egualmente allo studio. 4. Ledonne A., Federici M., Giustizieri M., Pessia M., Imbrici P., Millan M.J., Bernardi G., Mercuri N.B. (2010). Trace amines depress D2-autoreceptor-mediated responses on midbrain dopaminergic cells. British J. Pharmacol. 160, 1509-1520 (Article Online: Apr 1 2010; DOI: 10.1111/j.1476-5381.2010.00792.x; I.F.4.902). 5. Pessia M, Hanna M.G. (2010). Episodic Ataxia Type 1. Editors: Pagon R.A., Bird T.C., Dolan C.R., Stephens K. University of Washington, Seattle (WA). GeneReviews [Internet] (invited review). Available at: www.ncbi.nlm.nih.gov/bookshelf/ br.fcgi?book=gene&part=ea1). 6. Imbrici P., Grottesi A., D‘Adamo M.C., Mannucci R., Tucker S.J. and Pessia M. (2009). Contributions of the central hydrophobic residue in the PXP motif of Voltage-Dependent K+ Channels to S6 flexibility and Gating Properties. Channels (Austin) 3, 39-45.

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7. Imbrici P., Gualandi F., D‘Adamo M.C., Taddei Masieri M., Cudia P., De Grandis D., Mannucci R., Nicoletti I., Tucker S.J., Ferlini A. and Pessia M. (2008). A Novel KCNA1 Mutation Identified in an Italian Family Affected by Episodic Ataxia Type 1” Neuroscience 157, 577-587 (DOI: 10.1016/j.neuroscience.2008.09.022, published on line 24.09.2008). The front cover figure of Neuroscience (issue 157) was taken from this study. 8. Pessia M.*, Servettini I., Panichi R., Guasti L., Grassi S., Arcangeli A., Wanke E., Pettorossi V.E. (2008). ERG voltage-gated K+ channels regulate excitability and discharge dynamics of the medial vestibular nucleus neurons. J. Physiol. (London) 586, 4877-4890; I.F.4.764.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 32

BIOGRAPHICAL SKETCH Joseph P. Pillion Title: Ph.D. Director of Audiology

Date of Birth: 7/22/1949

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EDUCATION Institution and Location

Degree

Western Michigan University The Ohio State University The Ohio State University Johns Hopkins University School of Medicine

B.A. M.A. Ph.D. Poostdoctoral fellowship

Year Conferred

Scientific Field

Contact points [email protected]

Professional Appointments Assistant Professor, Department of Physical Medicine and Rehabilitation, Johns Hopkins School of Medicine

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Research and Professional Experience Adjunct Faculty, Distance Au.D. Program Department of Communication Disorders Central Michigan University Assistant Professor Department of Physical Medicine and Rehabilitation Johns Hopkins University School of Medicine Core Faculty in Audiology, MCHB Training Program; Leadership Education in Neurodevelopmental Disabilities, Kennedy Krieger Institute and Johns Hopkins University Post-Doctoral Fellowship in Audiology Department of Pediatrics Johns Hopkins University School of Medicine Research Associate The Ohio State University

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Publications during last three years Schmitz, J., West, K.P., Lee S-F Wu, Khatry, S.K., LeClerq, S.C., Karna, S.L., Katz, J., and Pillion, J.P. Preschool vitamin A supplementation and reduced risk of hearing loss among young adults in rural Nepal. The Lancet. In Submission. Wasserman, E.E., Nelson, K., Rose, N.R., Rhode, C., Pillion, J.P., Seaberg, E., Talor, M.V., Burek, L., Eaton, W., Duggan, A., and Yolken, R.H. Maternal Thyroid Autoimmunity, Childhood Hearing Loss and IQ in the Baltimore CPP. Under Revision for Pediatric Research. Pillion, J.P., Bibat, G., and Naidu, S. (2010). Effects of sedation on auditory brainstem response in Rett syndrome. Pediatric Neurology. 42, (5), 331-334. Schmitz, J. Pillion, J.P., LeClerq, S.C., Khatry, S.K., Lee S-F Wu, Prasad, R., Karna, S.L., Shrestha, S.R., and West, K.P. (2010). Prevalence of hearing loss and ear morbidity among adolescents and young adults in rural southern Nepal. International Journal of Audiology. 49, (5), 388-394. DiPietro, J.A., Kivlighan, K.T., Costigan, K.A., Rubin, S.E., Shiffler, D.E., Henderson, J.L., and Pillion, J.P. (2010). Prenatal antecedents of newborn neurological maturation. Child Development. 81, (1), 115-130. Wasserman, E.E., Nelson, K., Rose, N.R., Rhode, C., Pillion, J.P., Seaberg, E., Talor, M.V., Burek, L., Eaton, W., Duggan, A., and Yolken, R.H. (2009). Infection and autoimmunity: A seroepidemiologic study of TPOaAb. Autoimmunity. 42, 439-446. Pillion, J.P. and Shapiro, J. (2008). Audiological findings in osteogenesis imperfecta. Journal of the American Academy of Audiology. 19, 595-601.

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Pillion, J.P., Moser, H.W., and Raymond, G.V. (2008). Audiological findings in adrenomyleoneuropathy. Journal of the Neurological Sciences, 269, (1-2), 24-29. Wasserman, E.E., Nelson, K., Rose, N.R., Eaton, W., Pillion, J.P., Seaberg, E., Talor, M.V., Burek, L., Duggan, A., and Yolken, R.H. (2008). Maternal thyroid autoantibodies during the third trimester and hearing deficits in children: An epidemiologic assessment. American Journal of Epidemiology, 167, (6), 701-710. Pillion, J.P. Audiological assessment of infants and children with developmental disabilities. (2008). Book Chapter In: Capute and Accardo‘s Developmental Disabilities in Infancy and Childhood Volume II, 3rd Edition.. Edited by: P. Accardo: Paul H. Brookes, Baltimore, MD.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 33

BIOGRAPHICAL SKETCH Alessandra Quercioli Title: University Hospital of Geneva, Switzerland, Medical Specialties Departement

Date of Birth: 12.8.1980

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EDUCATION Institution and Location University of Genoa, Italy University of Genoa, Italy.

Degree Accomplishment of the MD title Accomplishment of the title of Specialist in Internal Medicine

Year Conferred 2005

Scientific Field

October 2010,

Contact points Address: Rue Gabrielle-Perret-Gentil, 4; 1211 Genève, Suisse.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 34

BIOGRAPHICAL SKETCH M. Dominique Sappey-Marinier Title: Associate Professor of Biophysics and Nuclear Medicine CERMEP – Imagerie du Vivant

Date of Birth: 29th August, 1959

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EDUCATION Institution and Location

Degree

Year Conferred

Montreal Mc Gill Univ.

Research collaboration

1997-2000

Habilitation for Direction of Research (HDR) UCB-Lyon1 UC San Francisco (VAMC) UCB-Lyon1 UCB-Lyon1

Scientific Field

1996 Post-doctorate Doctorat of Sciences (PhD) Master of Biomedical Imaging

1987- 1990 1987 1984

Contact points Groupement Hospitalier Est - 59, Boulevard Pinel, 69677 Bron, France Tél: 33 (0) 4 72 68 86 07 (00) Fax: 33 (0) 4 72 68 86 10 Email: [email protected]

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RESEARCH AND PROFESSIONAL EXPERIENCE Associate Professor of Biophysics and Nuclear Medicine Medical School Lyon-Est, University Claude Bernard – Lyon1 (UCB-Lyon1) CERMEP-Imagerie du Vivant, Hôpital Neurologique, Hospices Civils de Lyon CREATIS, UMR CNRS 5220 & U630 INSERM

Research Axis Development of MRI methodology for functional and metabolic brain applications

Positions 2010-… Head of MR Brain Imaging team of the CREATIS laboratory 2010-… President of French MR society named ―GRAMM‖ 2004-… Head of MRI department (CERMEP-Imagerie du Vivant) 2001-2005 Office Member of European ―Crystal Clear‖ Collaboration 1997-2000 Adjunct-Director of Network and ComputerCenter UCB-Lyon1 1993-… Associate Professor of Medicine UCB-Lyon1 1990-1993 Assistant Professor of Medicine UCB-Lyon1

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Main Publications 1. D. Sappey-Marinier, A. Briguet et J. Delmau: Perspectives d'Emploi de la Résonance Magnétique Nucléaire pour l'Etude Biochimique de la Substance Blanche Cérébrale. Arch. Int. Physio. Bioch. 93: 129-140, 1985. 2. D. Sappey-Marinier, R. Letoublon, and J. Delmau: Phosphorus NMR Analysis of Human White Matter in Mixed Nonionic Detergent Micelles. J. Lipid Res. 29: 1237-1243, 1988. 3. A.A. Maudsley, D.B. Twieg, D. Sappey-Marinier, B. Hubesch, J.W. Hugg, G.B. Matson, and M.W. Weiner: Spin Echo 31P Spectroscopic Imaging in the Human Brain. Magn. Reson. Med. 14: 415-422, 1990. 4. D. Sappey-Marinier: High Resolution NMR Spectroscopy of Cerebral White Matter in Multiple Sclerosis. Magn. Reson. Med. 15: 229-239, 1990. 5. D. Sappey-Marinier, B. Hubesch, G.B. Matson, and M.W. Weiner: Decreased Phosphorus Metabolites and Alkalosis in Chronic Cerebral Infarction. Radiology 182: 29-34, 1992. 6. D. Sappey-Marinier, R. Deicken, G. Fein, G. Calabrese, B. Hubesch, C. Van Dyke, D. Dillon, L. Davenport, D. Meyerhoff, and M.W. Weiner: Alterations in Brain Phosphorus Metabolite Concentrations Associated with Areas of High Signal Intensity White Matter at MR Imaging. Radiology 183: 247-256, 1992. 7. D. Sappey-Marinier, G. Calabrese, H.P. Hetherington, S. Fisher, R.F. Deicken, C. Van Dyke, G. Fein, and M.W. Weiner: Proton MRS of Human Brain: Applications to Normal White Matter, Chronic Infarction and MRI White Matter Signal Hyperintensities. Magn. Reson. Med. 26: 313-327, 1992.

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8. R.F. Deicken, G. Calabrese, J. Raz, D. Sappey-Marinier, B. Hubesch, M.W. Weiner, and G. Fein: A 31 Phosphorus Magnetic Resonance Spectroscopy Study of the Effect of Diazepam on Brain Phosphorus Metabolism. Biological Psychiatry 32: 628-631, 1992. 9. D. Sappey-Marinier, L. Chileuitt, M.W. Weiner, A.I. Faden, and P.R. Weinstein: Hypoglycemia Prevents Increase in Lactic Acidosis During Reperfusion After Temporary Cerebral Ischemia in Rats. NMR in Biomedicine 8: 171-179, 1995. 10. D.J. Meyerhoff, S. MacKay, D. Sappey-Marinier, R. Deicken, G. Calabrese, W.P. Dillon, M.W. Weiner, and G. Fein: Effects of chronic alcohol abuse and HIV infection on brain phosphorus metabolites. Alcoholism Clin. Exp. Res. 19: 685-692, 1995. 11. D. Sappey-Marinier, A. Vighetto, R. Peyron, E. Broussolle, A. Bonmartin: Phosphorus and Proton Magnetic Resonance Spectroscopy in patients with Episodic Ataxia of Type 2. Ann. Neurol. 46: 256-259, 1999. 12. E. Angelié, A. Bonmartin, AEO. Boudraa, PM. Gonnaud, JJ. Mallet, D. Sappey-Marinier: Regional Metabolism in Normal Aging of the Human Brain: A 1H MRSI Study. Am J Neuroradiol. 22: 119-127, 2001. 13. D. Sappey-Marinier, O. Beuf, C. Billotey, E. Chereul, J. Dupuy, M. Jeandey, D. Grenier, J. Hasserodt, JB. Langlois, C. Lartizien, W. Mai, C. Odet, J. Samarut, D. Vray, L. Zimmer, M. Janier. The Animage project: a multimodal imaging platform for small animal research. Nucl. Inst. Meth. Phys. Res. A 527: 117-123, 2004. 14. S. Narayanan, S.J. Francis, J.G. Sled, A.C. Santos, S. Antel, I. Levesque, S. Brass, Y. Lapierre, D. Sappey-Marinier, G.B. Pike and D.L. Arnold: Axonal injury in the cerebral normal-appearing white matter of patients with multiple sclerosis is related to concurrent demyelination in lesions but not to concurrent demyelination in normal-appearing white matter. NeuroImage, 29, 637-642, 2006. 15. Bagory M, Durand-Dubief F, Ibarrola D, Confavreux C, Sappey-Marinier D. "Absolute" quantification in magnetic resonance spectroscopy: validation of a clinical protocol in multiple sclerosis. Conf. Proc. IEEE Eng. Med. Biol. Soc. 3458-61, 2007. 16. J. Zyss, J. Xie-Brustolin, P. Ryvlin, S. Peysson, A. Beschet, D. Sappey-Marinier, M. Hermier, S. Thobois. Epilepsia partialis continua with dystonic hand movement in a patient with a malformation of cortical development. Mov Disord. Sep 15; 22(12): 17936, 2007. 17. HJ. Lee, E. Truy, G. Mamou, D. Sappey-Marinier, AL. Giraud. Visual speech circuits in profound acquired deafness: a possible role for latent multimodal connectivity. Brain. Nov; 130(Pt 11):2929-41, 2007. 18. D. Sappey-Marinier, M. Bagory, S. Hannoun, D. Ibarrola, C. Confavreux, F. DurandDubief. Characterization of Neurodegenerative Processes in Multiple Sclerosis using Magnetic Resonance Spectroscopic Imaging and Diffusion Tensor Imaging. Conf. Proc. MICCAI, 2008 19. S. Hannoun, F. Durand-Dubief, W. Jalalzai, Danielle Ibarrola, J.C. Comte, Christian Confavreux, and D. Sappey-Marinier. Caractérisation de la substance blanche apparement normale dans la sclérose en plaques par IRM de tenseur de diffusion. Ingeniérie et Recherche BioMédicale (IRBM), 30:179-183, 2009.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 35

BIOGRAPHICAL SKETCH Hans-Georg Schlosser Title: Priv.-Doz. Dr. med.

Date of Birth: 28 May 1971

EDUCATION Degree

Year Conferred

Scientific Field

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Institution and Location Universitätsmedizin Berlin, Klinik für Neurochirurgie

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Chapter 36

BIOGRAPHICAL SKETCH Nobuaki Shimoda Title: Ph.D.

Date of Birth: February 11, 1963

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EDUCATION Institution and Location

Degree

Year Conferred

Department of Occupational Therapy, National Sanatorium Tokyo Hospital Rehabilitation School, Japan Department of Sociology, School of Sociology, Bukkyo University, Japan Master‘s Program in Health Sciences,International University of Health and Welfare Graduate School, Japan Doctoral Program in Health Sciences,International University of Health and Welfare Graduate School, Japan

Diploma‘s Course

April 1985 March 1988

Bachelor‘s course Master‘s course

April 1994 March 1998 April 1999 March 2001

Doctoral Course

April 2001 March 2004

Scientific Field

Contact points Address: 2600-1, Kita-Kanemaru, Otawara, Tochigi, Japan Postal code 324-8501 Telephone: +81-287-24-3000 Email: [email protected]

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RESEARCH AND PROFESSIONAL EXPERIENCE April 1995 – present: Department of Occupational Therapy, International University of Health and Welfare, Otawara, Japan

Professional Appointments Associate Professor

Publications during last three years

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(1) Kotaro Takeda, Yukihiro Gomi, Itsuki Imai, Nobuaki Shimoda, Masao Hiwatari, Hiroyuki Kato: Shift of motor activation areas during recovery from hemiparesis after cerebral infarction: A longitudinal study with near-infrared spectroscopy. Neuroscience Research 59: 136-144, 2007. (2) Nobuaki Shimoda*, Kotaro Takeda*(*: These authors contributed equally to this research), Itsuki Imai, Junichiroh Kaneko, Hiroyuki Kato: Cerebral laterality differences in handedness: a mental rotation study with NIRS. Neurosci Lett 430: 43-47, 2008. (3) Kotaro Takeda *, Nobuaki Shimoda * (*: These authors contributed equally to this research), Yutaka Sato, Misao Ogano, Hiroyuki Kato: Reaction time differences between left- and right-handers during mental rotation of hand pictures. Laterality: Asymmetries of Body, Brain and Cognition 15: 415 – 425, 2009

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 37

BIOGRAPHICAL SKETCH Tetsuya Shimokawa Title: Associate Professor

Date of Birth: 4/26, 1970

EDUCATION

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Institution and Location University of Tokyo

Degree Ph.D.

Year Conferred

Scientific Field Economics

Contact points [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE I was a Research fellow (DC) of Japan Society for the Promotion of Science in 1997; Research fellow of Center for International Research on the Japanese Economy, the University of Tokyo in 1999; and was a Research fellow (PD) of Japan Society for the Promotion of Science in 2000. Now, I am an Associate Professor at the School of Management at Tokyo University of Science, Japan.

Honors Who's Who in the World 2011 (28th Edition)

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Publications Last 3 Years

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Tadanobu Misawa, Shinichi Shiomi, Kyoko Suzuki, and Tetsuya Shimokawa, (2010), A Brain-computer Interface for Purchase Decision-making, International Journal of Computational Science. Volume 4(2) 173-185. Tetsuya Shimokawa, Kyoko Suzuki and Satoru Takahashi, (2010), An agent-based approach to test the usefulness of the behavioral finance in real financial markets, International Journal of Computational Science. Volume 4(2) 199-217. Tetsuya Shimokawa, Kyoko Suzuki, Tadanobu Misawa, Kazuhiro Miyagawa, (2009), Predictability of Investment Behavior from Brain Information Measured by Functional Near-Infrared Spectroscopy: A Bayesian Neural Network Model, Neuroscience, 161, 347-358. Tetsuya Shimokawa, Kyoko Suzuki, Tadanobu Misawa, (2009), Augmented Reinforcement Learning and Investment Decision Making, NeuroComputing, Volume 72, Issues 16-18, 3447-3461 Kyoko Suzuki, Tetsuya Shimokawa, and Tadanobu Misawa, (2009), An Agent-based Approach to Option Pricing Anomalies, The IEEE Transactions on Evolutionary Computation, Volume: 13, Issue 1: 19-32 Tetsuya Shimokawa, Tadanobu Misawa, Kyoko Suzuki, (2008), Neural Representation of Preference Relationships, NeuroReport, 19(16):1557-1561.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 38

BIOGRAPHICAL SKETCH Amruthesh C. Shivachar Title: PhD Texas Southern University

Date of Birth:

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EDUCATION Institution and Location University of Mysore, India School of Medicine, Virginia Commonwealth University, VA 23298

Degree PhD Post-doc

Year Conferred

Scientific Field Biochemistry Pharmacology

Contact points Address: Department of Pharmaceutical Sciences, Texas Southern University, 3100 Cleburne Avenue, Houston, TX 77004

RESEARCH AND PROFESSIONAL EXPERIENCE Astrobiology, pharmacogenomics and Cannabinoid neuropharmacology

Professional Appointments 2009-date Associate Professor, Department of Pharmaceutical Sciences, College of Pharmacy, Texas Southern University, Houston, TX, 7704

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2002-2009 Assistant Professor, Department of Pharmaceutical Sciences, College of Pharmacy, Texas Southern University, Houston, TX, 7704 2002-2002 Visiting Scientist, Department of Cell Biotechnology, NASA-Johnson Space Center, Houston, TX 77585 1996-2002 Visiting Assistant Professor, Department of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX. 77042 1993-1996 Research Assistant Professor, Department of Pharmacology /Toxicology, Medical College of Virginia, Richmond, VA 23298. 1992-1993 Research Instructor, Department of Pharmacology /Toxicology, Medical College of Virginia, Richmond, VA 23298

Honors 1989: American Heart Association Research fellowship Award-Virginia Affiliate 2004: American Society of Neurochemistry Young Investigator Travel Award

Publications Last 3 Years

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Seema R, Morisseau C, Hammock BD, Shivachar, AC. Differential sub cellular distribution and co-localization of microsomal epoxide hydrolase and soluble epoxide hydrolase in cultured rat cortical astrocytes. J. Neurosci. Res. 87:218-227 2009 Shivachar A. C. Isolation and culturing of glial, neuronal and neural stem cell types encapsulated in biodegradable peptide hydrogel. Chapter 8 in Topics in Tissue Engineering, Vol 4. 2008, Eds. N. Ashammakhi, R. Reis and F Chiellini.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 39

BIOGRAPHICAL SKETCH Gen Sobue Title: M.D., Ph.D. Medicine

Date of Birth: March 2nd, 1950

Contact points [email protected]

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RESEARCH AND PROFESSIONAL EXPERIENCE Molecular science and clinical neurology

Professional Appointments Professor

Publications during last three years Koike H, Sobue G. Expanding the concept of inflammatory neuropathies. Brain 133: 284851, 2010. Sone J, Tanaka F, Koike H, et al. Skin biopsy is useful for the antemortem diagnosis of neuronal intranuclear inclusion disease. Neurology [in press] Koike H, Atsuta N, Adachi H, et al. Clinicopathological features of acute autonomic and sensory neuropathy. Brain 133: 2881-2896, 2010.

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Chapter 40

BIOGRAPHICAL SKETCH Keisuke Suzuki Title: M.D., Ph.D. Medicine

Date of Birth: February 14th, 1973

Contact points [email protected]

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RESEARCH AND PROFESSIONAL EXPERIENCE Clinical neurology

Professional Appointments Researcher

Publications during last three years Suzuki K, Katsuno M, Banno H, et al. The profile of motor unit number estimation (MUNE) in spinal and bulbar muscular atrophy. J Neurol Neurosurg Psychiatry 81: 567-571, 2010. Suzuki K, Katsuno M, Banno H, Sobue G. Pathogenesis-targeting therapeutics for spinal and bulbar muscular atrophy (SBMA). Neuropathology 29: 509-516, 2009.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 41

BIOGRAPHICAL SKETCH Feng Ru Tang Title: MD, Ph.D. Temasek Laboratories, National University of Singapore

Date of Birth: May 4, 1964

Contact points

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Address: Temasek Laboratories, National University of Singapore, 5A Engineering Drive 1, #06-27, Singapore 117411.

RESEARCH AND PROFESSIONAL EXPERIENCE Neuroscience, Epilepsy

Professional Appointments Senior Research Scientist

Publications during last three years: International Refereed Journals (*: Correspondence author)

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Ma DL, Tang YC, Tang FR*, Cytoarchitectonics and afferent/efferent reorganization of the lateral entorhinal cortex in the mouse pilocarpine model of temporal lobe epilepsy J. Neurosci. Res. 86(6) (2008):1324-1342. Kaur1 C., Sivakumar V., Lu J., Tang FR., Ling EA., Melatonin Attenuates Hypoxia-Induced Ultrastructural Changes and Increased Vascular Permeability in the Developing Hippocampus. Brain Pathology 18(4) (2008):533-47. Liu JX, Tang YC, Liu Y, Tang FR*. mGluR5-PLCβ4-PKCβ2/PKCγ pathways in hippocampal CA1 pyramidal neurons in pilocarpine model of status epilepticus in mGluR5+/+ mice. Epilepsy Res 82(2-3): 111-123. Zhang S, Khanna S, Tang FR*. Patterns of hippocampal neuronal loss and axon reorganization of the dentate gyrus in the mouse pilocarpine model of temporal lobe epilepsy J. Neurosci. Res. 87(5) (2009):1135-1149. Xu JH, Long L, Tang YC, Zhang JT, Hu HT, Tang FR*. CCR3, CCR2A and MIP-1α, MCP1 in the mouse hippocampus during and after pilocarpine induced status epilepticus. Neuropathology and Applied Neurobiology 35(5) (2009):496-514 Tang FR*, Bradford HF, Ling EA, Metabotropic glutamate receptors in the control of neuronal activity and as targets for development of anti-epileptogenic drugs. Curr Med Chem. 16(17) (2009):2189-204. (Invited review). Xu JH, Long L, Wang J, Tang YC, Hu HT, Soong TW, Tang FR*. Nuclear localization of Ca(v)2.2 and its distribution in the mouse central nervous system, and changes in the hippocampus during and after pilocarpine-induced status epilepticus. Neuropathol Appl Neurobiol. 36(1) (2010):71-85. He DF, Ma DL, Tang YC, Lee WL, Engel Jr. J, Bragin A, Tang FR*. Morpho-physiological characteristics of dorsal subicular network in mice after pilocarpine induced status epilepticus. Brain Pathol 20(2010): 80-95. Tang FR*, Loke WK. Cyto-, axo- and dendro-architectonic changes of neurons in the limbic system in the mouse pilocarpine model of temporal lobe epilepsy. Epilepsy Res.;89(1) (2010):43-51. Zhang S, Xia YY, Lim HC, Tang FR, Feng ZW. NCAM-mediated locomotor recovery from spinal cord contusion injury involves neuroprotection, axon regeneration, and synaptogenesis. Neurochem Int. 56(8)(2010): 919-29 Liu JX, Tang YC, Liu Y, Tang FR*. Catalytic subunits of PKA in the mouse hippocampus at the acute stage during and after pilocarpine-induced status epilepticus. Seizure 19(7)(2010): 414-420. Tang FR*, Loke WK, Ling EA. Pilocarpine-, Soman- and Sarin- Induced Seizures: Mechanism, Metabolic, Biochemical and Neuroinflammatory Changes and Current Therapeutic Approaches. Curr Med Chem. 18(6) (2011):886-99. Liu JX, Tang YC, Liu Y, Tang FR*. Pilocarpine induced status epilepticus alters hippocampal PKC expression in mice. Acta Neurobiologiae Experimentalis. (2011, in press).

Book Chapters Tang FR, Lee WL, Hippocampal mossy fiber reorganization in temporal lobe epilepsy (TLE). Chapter 3 in Pan Brain Abnormal Neural Network in Epilepsy (edited by Feng Ru Tang, Publisher: Research Signpost) Pg 23-40 (2009).

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Tang FR, Ma DL, Lee WL, Entorhinal cortex in temporal lobe epilepsy. Chapter 8 in Pan Brain Abnormal Neural Network in Epilepsy (edited by Feng Ru Tang, Publisher: Research Signpost), Pg 121-133(2009). Tang FR, Loke WK, Neurogenesis in the dentate gyrus of patients and animal models of temporal lobe epilepsy. Neurogenesis, Neurodegeneration and Neuroregeneration (edited by Bor LuenTang, Publisher: Research Signpost) pg 43-58( 2010). Book

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Tang Feng Ru, Pan-Brain Neural Network in Epilepsy, Research Signpost (as an Editor, and contributor for 2 Chapters) ( 2010).

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Chapter 42

BIOGRAPHICAL SKETCH Maria Victoria Tejada-Simon Title: Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, USA.

Date of Birth: November 7, 1964

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EDUCATION Institution and Location

Degree

Year Conferred

Michigan State University University of Houston

Master of Science Master of Education in Teaching PhD

1994 2007

Michigan State University

Scientific Field

1998

Contact points Address: 521 Science and Research, room 551, mail code 5037, College of Pharmacy, University of Houston, Houston, TX 77204

RESEARCH AND PROFESSIONAL EXPERIENCE 1998-2000 Postdoctoral Fellow - Professor J. Zhang, Department of Neurology. at Baylor College of Medicine (BCM), Houston, TX. 2001-2005 Instructor, Dpt. Molecular Physiology and Biophysics, BCM, Houston, TX. 2006 –2007 Assistant Professor, Dpt. Molecular Physiology and Biophysics, BCM, Houston, TX.

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2006-2007 Assistant Director of Postdoctoral training Program, Dpt. Molecular Physiology and Biophysics, BCM, Houston, TX. 2008-pres. Assistant Professor, Dpt. Pharmaceutical and Pharmacological Sciences, College of Pharmacy, University of Houston, Houston, TX. 2008-pres. Adjunct Assistant Professor, Dpt. Psychology, University of Houston, TX. 2009-pres. Adjunct Assistant Professor. Dpt. Biology. University of Houston, TX.

Professional Appointments 2008-pres. Assistant Professor, Dpt. Pharmaceutical and Pharmacological Sciences, College of Pharmacy, University of Houston, Houston, TX. 2008-pres. Adjunct Assistant Professor, Dpt. Psychology, University of Houston, TX. 2009-pres. Adjunct Assistant Professor. Dpt. Biology. University of Houston, TX.

Honors

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2000-Methodist Hospital Foundation Grant Award. Methodist Hospital. 2001-Federation of Clinical Immunology Society educational Award. 2006-Academy Distinguished Educators Education Award (BCM) 2007-Biotechnology Institute Fellow. The Biotechnology Institute. 2007-Academy Distinguished Educators Scholarship award (BCM) 2009-National Fragile X Foundation award 2009-Carl Storm Scholarship. GRC. 2010-FASEB-MARC Faculty-student award 2010-Finalist Sisley-LeJeune international award

Publications during last three years Hoeffer, C.A., Tang, W., Wong, H., Santillan, A., Patterson, R.J., Martinez, L.A., TejadaSimon, M.V., Paylor, R., Hamilton, S.L., and Klann, E. (2008). Removal of FKBP12 enhances mTOR/Raptor interactions, LTP, memory, and perseverative/repetitive behavior. Neuron, 60(5):832-845. Elhardt, M.E.; Martinez, L.A.; Tejada-Simon, M.V. (2010). Neurochemical, behavioral and architectural changes after chronic inactivation of NMDA receptors in mice. Neurosci. Let., 468(2):166-171. Salim, S.; Sarraj, N.; Taneja, M.; Saha, K.; Tejada-Simon, M.V.; Chugh, G. (2010). Moderate treadmill exercise prevents oxidative stress-induced anxiety-like behaviors in rats. Behav. Brain Res. 208(2):545-552.

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Martinez, L.A.; Tejada-Simon, M.V. (2011). Pharmacological inactivation of the small GTPase Rac1 impairs long-term plasticity and memory in the mouse hippocampus. Neuropharmacol., 61:305-312. Bongmba, O.Y.N.; Martinez, L.A.; Elhardt, M.E.; Butler, K.; Tejada-Simon, M.V (2011). Modulation of dendritic spine and synaptic function by Rac1: A possible link to Fragile X syndrome pathology. Brain Res. doi:10.1016/j.brainres.2011.05.020.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 43

BIOGRAPHICAL SKETCH Stefan Van der Mussele Title: University of Antwerp

Date of Birth: 06/10/1981

EDUCATION

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Institution and Location MNSc

Degree

Year Conferred

Scientific Field

Contact points Address: Universiteitsplein 1, 2610 Antwerp, Belgium

RESEARCH AND PROFESSIONAL EXPERIENCE Dementia, BPSD, Alzheimer‘s disease, frontotemporal dementia, MCI

Professional Appointments PhD student

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 44

BIOGRAPHICAL SKETCH Brankica Vasiljevic Title: Institute of Gynecology and Obstetrics-Clinical Centre of Serbia, Department of Neonatology, 26 Viðegradska Street, 11 000 Belgrade, Serbia

Date of Birth: 14.05.1962

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EDUCATION Institution and Location School of Medicine, University of Belgrade Serbia Yugoslav School of UltrasoundPaediatric Ultrasound Paediatrics, specialisation School of Medicine University of Belgrade Serbia Master of Science Medicine (MSc) School of Medicine University of Belgrade Serbia Neonatology, subspecialisation School of Medicine, University of Belgrade Serbia School of Medicine University of Belgrade Serbia

Degree MD

Year Conferred 1989

Scientific Field

1994 1997

1999

2004

PhD

2011

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Contact points Address: 2 Sime Igumanova Street, 11 000 Belgrade

Jobs held 1991-1992 Belgrade General Hospital General practice 1993-1999 Employed at University Children's Hospital, Belgrade Department of Haematology & Oncology 2000- Employed at Institute of Gynaecology & Obstetrics - University Clinical Centre, Belgrade Department of Neonatology-NICU

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Training 1992-1997: University Children‘s Hospital – Belgrade 1995: Institute of digestive disease - University Clinical Centre-Belgrade 2003: Institute for mother and child – Belgrade 2004: Institute of neonatology - Belgrade 2004: Alexander Hospital, Iaso Hospital and Elena Hospital - Athens 2007: Salzburg Medical Seminar – Maternal & Infant Health 2008: General Hospital of Salzburg - Internship in Neonatal Intensive Care 2008: Morgan Stanely Children‘s Hospital of New York-Presbyterian- Columbia University New York

Trial & Study Participation 1998: SIOP 93-01 protocol 1999: Intercontinental study group on Childhood – ITP 2003: INIS - International Neonatal Immunotherapy Study 2008: Twin Birth Study

Honors The ESPNIC Educational Grant, Geneva 2007

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Publications during last three years Vasiljevic B, Maglajlic-Djukic S, Gojnic M, Stankovic S, Ignjatovic S, Lutovac Dragana. New insights in the pathogenesis of perinatal hypoxic-ischemic brain injury. Pediatrics International PED-3290- In press doi: 10.1111/j.1442-200X.2010.03290.x Vasiljevic B, Maglajlic-Djukic S,Stankovic S, Ignjatovic S, Lutovac D, Gojnic M. Neonatal hypoxic-ischemic brain injury. BMJ 2011; (Published 19 January 2011 as Rapide Response to 340:doi:10.1136/bmj.c363) www.bmj.com/content/340/ bmj.c363/reply Gojnic M, Dugalic V, Brankovic M, Stojanovic I, Acimovic, M, Vasiljevic B. Is insulindependent diabetes and obesity a predisposition for endometrial and pancreatic carcinoma? Clinical and Experimental Obstetrics and Gynecology 2010; 37 (2):152-154 Vasiljevic B, Antonovic O, Maglajlic-Djukiã S, Gojniã M. The serum level of C reactive protein in the neonatal sepsis. Srp Arh Celok Lek 2008;131(5-6):253-8. Vasiljevic B, Gojnic M, Maglajlic-Djukiã S, Antonovic O. Normal values of cerebral blood velocities in the neonates. Srp Arh Celok Lek 2010; 138 (3-4):186-91. Vasiljevic B, Maglajlic-Gjukic S, Stankovic S, Dragana Lutovac, Gojniã M. Predictive value color Doppler ultrasonography for adverse neurodevelopment outcome in neonates with hypoxic-ischemic encephalopathy. Vojnosanit Pregl 33/2010- In press Vasiljevic B, Maglajlic-Djukic S, Gojnic M, Stankovic S. The Role of Oxidative Stress in Perinatal Hypoxic-Ischemic Brain Injury. Srp Arh Celok Lek192/2010-In press Vasiljeviã B, Maglajlic-Djukiã S, Gojnic M. The prognostic value of amplitude-integited electroencephalography in determination of neurodevelopment prognosis in neonates with hypoxic-ischemic encephalopathy. Vojnosanit Pregl 335/2010- In press Vasiljevic B, Stankovic S, Maglajlic Djukic S, Ignjatovic S, Lutovac D, Gojnic M, Bogicevic M. Assessment and influence neuroinflammation reaction in perinatal hypoxic–ischemic brain injury. Early Hum Devel 2010;86:S32. doi:10.1016/ j.earlhumdev.2010.09.088 Vasiljevic B, Gojnic M, Antonovic A, Lutovac D, Ignjatovic S, Maglajlic Djukic S. The prediction of adverse neurodevelopmental outcome after perinatal asphyxia using neuron specific enolase, cerebral function monitor and color Doppler ultrasonografy. Acta Pediatrica 2009; 98(sippl 460):258-9. Gojnic M, Brankovic M, Vasiljevic B, Fazlagic A, Dugalic S. Fetus compensation of high resistence by makeing aneurism. J Matern Fetal Neonatal Med 2008; 21 (suppl):136-7. Gojnic M, Fazlagic A, Vasiljevic B, Sparic R, Babovic I, Jeremic K, Arsenijevic Lj. Speed evolution in fetus maturation therapy. J Matern Fetal Neonatal Med 2008; 21 (suppl):156-7. Gojnic M, Dugalic S, Pervulov M, Brankovic M, Vasiljevic B, Antic M, Jeremic K, Micic L, Adamsons K. Using ordinary hematocrit level in prediagnosing preeclampsia. J Matern Fetal Neonatal Med 2008; 21 (suppl):270-1.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 45

BIOGRAPHICAL SKETCH Viroj Wiwanitkit Title: M.D. Wiwanitkit House, Bangkhae, Bangkok Thailand; visiting university professor, Hainan Medical University, China

Date of Birth:

Contact points

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Address: Wiwanitkit House, Bangkhae, Bangkok Thailand10160

RESEARCH AND PROFESSIONAL EXPERIENCE Laboratory medicine, tropical medicine, informatics

Professional Appointments University professor

Honors University professor

Publications Last 3 Years More than 400 papers

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 46

BIOGRAPHICAL SKETCH Jiann-Ming Wu Title: Associate Professor, Department of Applied Mathematics, National Dong Hwa University

Date of Birth: 1966.11.22

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Contact points Department of Applied Mathematics, National Dong Hwa University, Shoufeng, Hualien 974, Taiwan Tel.: +886 3 8633531; fax: +886 3 8633510. E-mail address: [email protected] E-mail address: [email protected]

RESEARCH AND PROFESSIONAL EXPERIENCE Current research interests include neural networks and signal processing. In the past decade, the author has developed effective learning methods for neural networks toward solving ICA, self-organization, classification, data driven function approximation and density estimation.

Publications Last 3 Years 1. Pei-Hsun Hsu and Jiann-Ming Wu, Book: Function approximation using generalized adalines, VMD Verlag, March, 2010. 2. Jiann-Ming Wu, Multilayer Potts perceptrons with Levenberg-Marquardt learning, IEEE Transactions on Neural Networks, Vol. 19, No. 12, December 2008(SCI)

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3. Jiann-Ming Wu, M.H. Chen, Lin Z.H., Independent component analysis based on marginal density estimation using weighted Parzen windows, Neural Networks 21 (2008) pp. 914924 (SCI) 4. Jiann-Ming Wu, Fetal electrocardiogram extraction by annealed expectation maximization, Neurocomputing 71, pp 1500-1514, 2008(SCI) 5. Jiann-Ming Wu, Hsiao-Chang Chen, Chun-Chang Wu, and Pei-Hsun Hsu, Blind image deconvolution by recursive function approximation, Singapore, International Conference on Signal and Image Processes, August, 2010 (EI, Compendex). 6. Jiann-Ming Wu, Hsiao-Chang Chen, J.C. Wu, Pei-Hsun Hsu, Blind image deconvolution by neural recursive function approximation, World Academy of Science, Engineering and Technology, 2010 7. Jiann-Ming Wu†, Shih-Hua Lee, Convolutive independent component analysis by leaveone-out optimal kernel approximation, the 6th international conference on Computing, Communications and Control technology 2008, in the context of The International MultiConference on Engineering and Technological Innovation: IMETI 2008, June 29th - July 2nd, 2008 Orlando, Florida, USA

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 47

BIOGRAPHICAL SKETCH Wandong Zhang Title: MD., Ph.D. Senior Research Officer; Adjunct Professor

Date of Birth: Aug. 11, 1959

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EDUCATION Institution and Location

Degree MD

Year Conferred 1982

Scientific Field Medicine

Southeast University School of Medicine, China Southeast University School of Medicine, China Molecular Biology & Genetics, University of Guelph, Canada Certificate for the United States Medical Licensing Examinations issued by the Educational Commission for Foreign Medical Graduates (USA)

M. Sci.

1986

Pathology

Ph.D.

1994

MD License in USA

CONTACT POINTS 1200 Montreal Road, Building M54 Ottawa, Ontario, Canada K1A 0R6 Tel: 1-613-993-5988 (work) Fax: 1-613-941-4475 (work) E-mail address: [email protected]

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RESEARCH AND PROFESSIONAL EXPERIENCE Senior Research Officer Project Leader Neurobiology Program Institute for Biological Sciences National Research Council of Canada, Ottawa, Ontario, Canada Adjunct Professor Department of Pathology and Laboratory Medicine Department of Cellular & Molecular Medicine Faculty of Medicine University of Ottawa, Canada

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Selected Peer-Reviewed Publications in last three years Shen S, Callaghan D, Juzwik C, Xiong H, Huang P, Zhang W. 2010. ABCG2 reduces ROSmediated toxicity and inflammation: A potential role in Alzheimer's disease. J Neurochem. 114(6): 1590-1604. Shen S, Zhang W. 2010. ABC transporters and drug efflux at the blood-brain barrier. Rev Neurosci. 21(1):29-53. Xiong H, Callaghan D, Bai J-Y, Jones A, Rasquinha I, Smith C, Walker D, Lue L-H, Stanimirovic DB, D, Zhang W. 2009. ABCG2 is up-regulated in Alzheimer‘s brain with cerebral amyloid angiopathy and may act as a gatekeeper at the blood-brain barrier for Aβ1-40 peptides. Journal of Neuroscience 29(17): 5463-5475. Vukic V, Callaghan D, Walker D, Lue L-H, Liu Q-Y, Stanimirovic DB, Zhang W. 2009. Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer‘s brain is mediated by the JNK-AP1 signaling pathway. Neurobiology of Disease. 34: 95-106. Zhang W, Wu J, Li Y, F-S Li, Njoo H. 2009. Rapid and accurate in vitro assays for detection of West Nile virus in blood and tissues. Transfusion Med. Rev. 23(2): 146-154. Xiong H, Callaghan D, Jones A, Walker D, Lue L-H, Woulfe J, Beach TG, Sue L, Xu H, Stanimirovic D, Zhang W. 2008. Cholesterol retention in Alzheimer‘s brain is responsible for high J3-and y-secretase activities and AJ3 production. Neurobiology of Disease 29: 422-437. Zhang W. 2008. Cholesterol, secretase activities, and AJ3 production in Alzheimer‘s pathogenesis. Cognitive Sciences 3(2): 201-221. Zhang, W. 2008. Impaired brain cholesterol homeostasis and Alzheimer‘s disease. Trends in Neurosciences. 5: 487-503 (Higher Education Press, Beijing, in press) Zhang, H., Zhang, W., Li, F. 2008. Prognostic significance of MDR-1 P-glyco-protein expression in breast cancer. J. Nanjing Medical University (ELSEVIER, English) 22(3): 148-152 (corresponding author). Zhang W, Wu J, Li Y, Clarke CC, Wong T. 2008. The in vitro bioassay systems for amplification and detection of abnormal prion PrPSc in blood and tissues. Transfusion Med. Rev. 22(3): 234-242.

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Callaghan, D., Vukic, V., Giuseppin, S., Jones, J., Walker, D., Lue, L-F., Woulfe, J., Chang, N., Beach, T.G., Sue, L., Stanimirovic, D., Zhang, W. 2007. Expression and regulation of inflammatory genes in human cerebrovascular endothelial cells induced by A peptides. In: Alzheimer’s Disease: New Advances, pp.83-86, Eds. Iqbal K., Winblad B., and Avila J., Medimond S.R.L, Bologna, Italy. Mojsilovic-Petrovic J, Callaghan D, Cui H, Dean C, Stanimirovic D, Zhang W. 2007. Hypoxiainducible factor-1 (HIF-1) is involved in the regulation of hypoxia-stimulated expression of monocyte chemoattractant protein-1 (MCP-1) and MCP-5 in astrocytes. J. Neuroinflammation 4:12. Fan R-H, Chen P-S, Zhao D, Zhang W. 2007. Hypoxia induced by CoCl2 influencing the expression and the activity of matrix metalloproteinase-2 in rat hepatic stellate cells. Chin. J. Hepatol. 15(9): 654-657. Zhang W, Mojsilovic-Petrovic J, Callaghan D, Jones A, Cui H, Howlett C, Stanimirovic D. 2006. Evidence that hypoxia-inducible factor-1 (HIF-1) mediates transcriptional activation of Interleukin-1J3 (IL-1J3) in astrocyte cultures. J. Neuroimmunology 174: 6373.

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PART 2 - RESEARCH SUMMARIES IN NEUROSCIENCE

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 48

A SYSTEM ARCHITECTURE APPROACH TO THE BRAIN: FROM NEURONS TO CONSCIOUSNESS L. Andrew Coward Department of Computer Science, Australian National University, Canberra, Australia

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RESEARCH SUMMARY This book is the integrated presentation of a large body of work on understanding the operation of biological brains as systems. The work has been carried out by the author over the last 22 years, and leads to a claim that it is relatively straightforward to understand how human cognition results from and is supported by physiological processes in the brain. This claim has roots in the technology for designing and manufacturing electronic systems which manage extremely complex telecommunications networks with high reliability, in real time and with no human intervention. Such systems perform very large numbers of interacting control features. Although there is little direct resemblance between such systems and biological brains, the ways in which these practical considerations force system architectures within some specific bounds leads to an understanding of how different but analogous practical considerations constrain the architectures of brains within different bounds called the Recommendation Architecture. These architectural bounds make it possible to relate cognitive phenomena to physiological processes.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 49

ADAPTIVE MECHANISMS IN MIGRAINE Vinod Kumar Gupta Dubai, United Arab Emirates

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Migraine has evolved into a giant puzzle and its literature comprises a vast loosely linked enterprise challenging human problem solving capacity. There is no central idea in migraine to elaborate a general theory which in turn could ultimately lead to creation of a unifying hypothesis that collects the various strands of evidences into a coherent and logically defensible intelligible synthesis. Current pathogenetic concepts of migraine, in particular cortical spreading depression (CSD), do not focus on the precise onset of the attack. Neither the aura nor the headache represents the true beginning of a migraine attack. The primary or causal physiological alteration underlying migraine lies in the ‗pre-prodromal‘ phase, the variable interim between exposure to the headache-provoking stimulus or situation and the onset of the migraine prodrome. The migraine prodrome itself can last several hours to a few days. Since CSD is believed to underlie both the migrainous scintillating scotoma as well as the headache, it cannot be regarded as an early or initial ‗pre-prodromal‘ physiological event. The biology of migraine is not the study of laboratory ‗markers‘ but the elucidation of physiological forces (trait and/or state factors) that push (precipitate) or pull (predispose) patients towards aura/headache or aura/headache-free state. The pathophysiology of migraine has been hitherto confined to analyses of diverse precipitating and remitting factors and uncertain postulations about recorded laboratory aberrations into presumptive causal algorithms. The key cranial physiological system involved in migraine remains unidentified. Migraine attacks occur during stress and, more commonly, after cessation of stress. The author has earlier proposed that a physiological neuroendocrine ‗system‘ comprised of wellregulated parallel activation of the vasopressinergic, intrinsic brain serotonergic, and intrinsic brain noradrenergic systems constitutes an important adaptive mechanism that governs vascular integrity, antinociception, behavior and overall function during stressful occasions, including migraine attacks. Such a conceptual template can be used to segregate the vast phenomenology of migraine into primary pathogenetic or secondary non-pathogenetic

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160

Vinod Kumar Gupta

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divisions; non-pathogenetic migrainous phenomena can be further subdivided into adaptive and concomitant (epiphenomenal) physiological events. Nausea and/or vomiting, facial pallor, Raynaud‘s phenomenon, episodic daytime sleepiness, and relative hypotension (both spontaneous as well as induced by prophylactic anti-migraine pharmacologic agents) likely reflect the non-pathogenetic (adaptive or epiphenomenal) clinical components of migraine. The pathophysiological basis of aura/headache and nausea/vomiting of migraine is very unlikely to be identical. Exogenous magnesium does not readily cross the intact blood-brain barrier and decreases the permeability of the blood-brain barrier. Magnesium depletion appears to serve an important adaptive function; its utility in migraine management is not convincing. Magnesium depletion, platelet activation, peripheral alterations in serotonin and catecholamine metabolism, hyper-responsiveness of brain noradrenergic, serotonergic, vasopressinergic, and dopaminergic systems, parasympathetic nevous system activation, pupillary miosis, and cutaneous allodynia probably represent some of the secondary adaptive physiological mechanisms operative in migraine. A critical or central role for brain neuronal involvement in migraine pathogenesis appears unikely as established migraine preventive agents like atenolol, nadolol, and verapamil do not readily cross the intact blood-brain barrier or influence brain neuronal function. Antidepressants, including amitriptyline, induce brain noradrenergic and serotonergic hyperfunction, rendering highly unlikely that such brain states underlie migraine. Elucidation of adaptive physiological mechanisms in migraine can rationalize important epidemiological, clinical, and pharmacological features and sow the seeds for evolution of an integrative synthesis which process, in turn, might herald the creation of a comprehensive thought framework and research vision for migraine.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 50

ANOTHER VIEW OF THE BRAIN SYSTEM Toshifumi Kumai Dept. of Oral & Maxillofacial Biology, Matsumoto Cental Univ., Japan

Shibukawa Yoshiyuki Dept. of Physiology, Tokyo Dental College / Brain Research Laboratory, Oral Health Science Center, Tokyo Dental College, Japan

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Our intelligent life deeply depends on the highly evolved nervous system of the brain, and the brain is one of most exciting themes in science. The authors have studied the control mechanism of the central nervous system in masticatory movements using electromyograms (EMG), electroencephalograms (EEG), and magnetoencephalograms (MEG). Much of the volume of this book is made up of descriptions of common established knowledge in neurophysiology, whereas short columns, entitled "A Different Angle‖, are interspersed here and there in each chapter. "A Different Angle" columns were based on students‘ questions. Many readers of this book may have had questions like those described in "A Different Angle" at an early stage of their study of neuroscience, but which may have been forgotten. Everybody, including specialists in neuroscience, will be able to read and use this book to gain a better understanding of the field.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 51

BASAL GANGLIA AND THALAMUS: THEIR ROLE IN COGNITION AND BEHAVIOUR Rita Moretti, Paola Torre and Rodolfo M. Antonello Clinca Neurologica dell 'Universita degli Studi de Trieste, Trieste, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The basal ganglia are traditionally involved in the control of movement. The most wise and prophetical works by Crossen (1996 and successive), and by Bogousslavsky stated clearly that the basal ganglia participate in multiple circuits or 'loops' with cognitive areas of the cerebral cortex; moreover, the activity of neurons within selected portions of the basal ganglia is more related to cognitive or sensory operations than to motor functions. Selection of phonological strings and morphological activities are clearly under the processation of basal ganglia loop. Moreover, automatic language is strictly bound to caudate and putamen articulatory and semnatic loop. Finally, in some instances basal ganglia lesions cause behaviour disturbances, such as apathia and the so called, frontal anterior syndrome, as well as palypsychism. In this the authors review these data, present experimental data, and detect the possible anatomical and functional framework for understanding the basal ganglia contributions to nonmotor function.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 52

BIOGENIC AMINES: PHARMACOLOGICAL, NEUROCHEMICAL AND MOLECULAR ASPECTS IN THE CNS Tahira Farooqui Aronoff Laboratory, Ohio State University, Columbus, OH, US

Akhlaq A. Farooqui Ohio State University, Columbus, OH, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Biogenic amines are naturally occurring amines that are derived by enzymic decarboxylation of the natural amino acids. They belong to a class of neurotransmitters including catecholamines (dopamine, norepinephrine, and epinephrine), indolamine (serotonin), and imidazoleamine (histamine). Biogenic amines have great pharmacological and physiological importance. The main objective of this book is to present readers with comprehensive information on pharmacology, neurochemistry and molecular neurobiology of biogenic amine in the CNS of vertebrate and invertebrates in a single volume text. The book has been organized into chapters and sections to provide a better flow of information. Furthermore, this unique volume provides its readers with cutting edge information on biogenic amines. It can be used by graduate students, postdoctoral fellows, researchers, and scientists who work at the pharmaceutical industry as a handbook, which describes all aspects of biogenic amine metabolism.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 53

BRAIN AND DISSOCIATED MIND Petr Bob Dept. of Psychiatary, Charles Univerity, First Faculty of Medicine, Prague, Czech Republic

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY This book presents current knowledge regarding relationship between conscious and unconscious processes in the human mind and dissociation between them, in a close relationship with modern neuroscientific research. Following the framework of traditional psychological and psychiatric terms proposed by Janet and developed also by Freud and Jung, the author shows new connections between modern theoretical neuroscience and psychological concept of dissociated mind. As main argument for this synthesis the author uses modern chaos theory that provides conceptual framework for self-organization that connect mind and brain. In this context the author also deals with the problem of consciousness and other interesting connections and mysteries of the human mind such as dreaming, hypnosis or pain experience.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 54

CEREBRAL BLOOD FLOW REGULATION Nodar P. Mitagvaria Inst. of Physiology, Tbilisi, Georgia

Haim (James) I. Bicher Valley Cancer Institute, Los Angeles, CA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Studies of the mechanisms relating blood supply to the brain appeared to be, in some sense, at a deadlock. Despite extensive application of different methodical approaches, no qualitative progress has been observed in these studies at the present time. This is perhaps due to the traditional, but not understandable, separation of neurophysiological and "circulatory" studies. It may seem very paradoxical, but the study of cerebral blood circulation proceeds almost in complete isolation from the knowledge about brain functions and does not take into account the specificity of the working brain as a part of the whole body. This book comprehensively addresses the issues of blood flow regulation. It is well known that the brain belongs to the group of organs having a high level of oxygen consumption. Oxygen consumption by the brain is an average 4.6 ml per 100 g of tissue per minute. In humans, the level of oxygen consumption by the whole brain attains 46 ml/min. This makes up approximately 20% of the total oxygen volume consumed by the organism. Consequently, the cerebral tissue is characterized by highly energetic processes. There is evidence indicating that even in functionally resting conditions, 18% of the entire energy expenditure of the body is utilized by the brain Calculations made by Rushmer indicate that the intensity of energy consumption by the human brain appears to be on average 20 Watt.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 55

CEREBRAL ISCHEMIA IN YOUNG ADULTS: PATHOGENIC AND CLINICAL PERSPECTIVES Alessandro Pezzini and Alessandro Padovani Brescia University Medical School, Brescia, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The literature concerning cerebral circulation, its control, its relation to the metabolism of the brain and its disorders, including cerebral ischemia, is very large and reflects an interest which goes back to Greek and Arabian medicine and which has greatly intensified, particularly over the past decades. Data of the literature remain, however, too sparse to propose a pragmatic approach to cerebral ischemia when affecting people at young age. The first purpose of this monograph has been therefore to bring together from such a literature a coherent account of how present concepts and approaches have developed. In this, the authors have been guided by what seems to be the important lines of investigation. Secondly, the evidence from studies which form the basis of the present understanding has been reviewed critically and, where possible, an attempt has been made to pose present controversies in terms which would be helpful in everyday clinical practice.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 56

COGNITIVE IMPAIRMENT IN CHILDREN WITH ADHD Alasdair Vance, Catherine Mollica and Paul Maruff University of Melbourne, Melbourne, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY There is limited understanding of the problems associated with repeated neuropsychological assessment in children, including the statistics used to guide decisions about cognitive change. Further, clinicians rarely consider change in cognitive function when evaluating treatment response in individual children with ADHD. This is most likely due to a lack of suitable assessment tasks as well as clinicians‘ limited awareness of the appropriate statistical techniques for measuring cognitive change in individuals. This book outlines a study investigating the application of a statistically principled decision rule to the cognitive and behavioural measures of individual children with ADHD in order to classify a significant, positive response to medication.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 57

COGNITIVE VISUAL MEMORY IN CATS V. M. Okujava and T. A. Natishvili Research Center for Experimental Neurology, Tbilisi, Georgia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The role of cognitive memory in ―becoming‖ of the complexly organized systems is briefly considered from the viewpoint of the general systems theory; the role of Georgian neurophysiologists in emphasizing cognitive aspects of memory role in animal behavior is underlined. The existence of the ―one-trial‖ nonspatial visual recognition memory in cats, as representatives of carnivores with poorly developed vision, is established; it is shown that analogously to primates and rodents in cats the so called rhinal cortex plays a major role in mediating this type of visual cognitive memory. It is shown that in cats, similarly to primates and rodents, parahippocampal cortex (with possible inclusion in this system of the subicular complex) is responsible for visuospatial memory. This new book examines the aspects of cognitive visual memory in cats.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 58

COGNITIVE-BEHAVIORAL AND NEUROPSYCHOLOGICAL MODELS OF OBSESSIVE-COMPULSIVE DISORDER Claudio Sica, Luigi Rocco Chiri University of Firenze, Italy

Dean McKay Fordham University, NY, US

Marta Ghisi

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

University of Padova, Italy

RESEARCH SUMMARY Obsessive compulsive disorder (OCD) is characterized by persistent, intrusive, and distressing obsessions (unwanted thoughts, impulses, or images) that may or may not be accompanied by compulsions (repetitive behaviors or mental acts). It is a severe and persistent psychological problem with significant negative effects on the individuals‘ social, family, and occupational functioning. This book reports on recent research examining phenomenology, neurobiology, psychological models, and computational modeling of obsessive-compulsive disorder. This book offers a general view of the most recent psychological and neurobiological research on OCD to researchers, psychologists, psychiatrists, mental-health professionals and students.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 59

CULTURAL AND LINGUISTIC INFLUENCE ON DEVELOPMENTAL NEURAL BASIS OF THEORY OF MIND: WHORFIAN HYPOTHESIS REVISITED Chiyoko Kobayashi Frank Fielding Graduate University, Santa Barbara, CA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Theory of mind (ToM) is defined as ability to understand mental states of others. ToM has been hypothesized to be a universal ability. However, several cross-cultural studies that examined non Anglo-American children found some variations in the onset time of ToM. Likewise, several recent brain imaging studies found variations in brain regions that are involved in ToM. These results suggest that ToM and its neural basis are not entirely universal and that there are some significant cultural / linguistic influences in the ToM development. In this book results of behavioral and neuroimaging studies that examined ToM and related social cognition are selectively reviewed. More specifically, the author discusses the roles of the medial prefrontal cortex and temporo-parietal junction that have been implicated in ToM and distinguishing ―self‖ from ―others‖. These structures may be particularly important for culture-dependent ways of ToM understanding. Theoretically, these results may support the Sapir-Whorf hypothesis: the person‘s language / culture sculpts his / her thoughts and cognition.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 60

DEVELOPMENTAL NEUROTOXICITY OF PBDES, MECHANISMS AND IMPLICATIONS Henrik Alm and Birger Scholz Uppsala University, Sweden

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY We are constantly exposed to a plethora of different chemicals, the majority of which are mostly uncharacterized with respect to their biological properties. This book provides an in depth overview on known neurotoxicity mechanisms for a group of industrial chemicals known as polybrominated diphenyl ethers (PBDEs). Polybrominated diphenyl ethers (PBDEs) are ubiquitous environmental toxicants that have been found world-wide in a variety of biotas. This new book reports and discusses the interesting and salient work published on the known and potential mechanisms behind the developmental neurotoxicity of PBDEs in the foremost used model organisms, mouse and rat.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 61

ELECTROMAGNETIC MIND CONTROL: FACT OR FICTION? A SCIENTIFIC VIEW V. N. Binhi General Physics Institute, Russian Academy of Sciences, Moscow, Russia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Although there are many publications in newspapers and popular magazines, discussing "Electromagnetic Mind Control" and "Electromagnetic Weapons," it is almost impossible to find reliable information on these issues, particularly where relatively weak electromagnetic (EM) radiations are of concern. This book fills the gap. Written for a general audience, it discusses the physics of and related scientific information on brain control using EM fields. It provides a balanced scientific viewpoint on the possibility of the effects of EM on the human brain and mind. The book considers     

current methods of EM information extracting from and delivery into the human brain general theoretical principles of EM field interactions with living objects modern experiments, including neurological ones the microwave hearing effect and technical limitations of the targeted exposure of humans to EM fields methodological limitations regarding EM mind control

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 62

EXPERIMENTAL ANIMAL MODELS IN NEUROBEHAVIORAL RESEARCH Allan V. Kalueff and Justin L. LaPorte Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Behavioral research has been an exciting staple of the neuroscientific community's efforts in combating the rising challenges of mental healthcare. New innovations are bringing a greater understanding of the pathogenic mechanisms behind the disorders and allowing for progress towards their remedies. this translantial approach, using newly developed animal modes, is of critical importance for the study of neuropsychiatric disorders. While the differences between the subjects of clinical research and basic research are obvious, there are many neurobiological similiarites that allow for the possibility of creating an accurate animal analogue of a human disorder. These tools contribute to translational research and are the best hope for countering the challenges facing the field of mental health. This book provides chapters on a range of issues in biopsychology and behavorial neuroscience. It offers innovative methodological and conceptual advances regarding topics such as sleep, depression, and anxiety, as well as how these domains interact. All authors of the book are recognized experts in the field, and have written their chapters for an international audience of basic and clinical neuroscientists who are interested in behavioral neurophenotyping. The writing will also be accessible to students at the undergraduate level, while still providing an important update to graduate students and professional researchrs in the disciplines of psychology, biology, and neuroscience on this rapidly developing field.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 63

ISOFLAVONES: A RACE AFTER THE RESCUE OF THE AGING HIPPOCAMPUS Catherine Bennetau-Pelissero, Khalid Jamali and Aline Marighetto Université de Bordeaux, UMRS, ENITA de Bordeaux, Gradignan, France

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Isoflavones are naturally occurring molecules present in significant amounts in many leguminous, some of which are edible plants. Isoflavones exhibit similarities in their chemical structure with steroidal estrogens, which allows them to trigger some of the endogenous physiocellular signalization processes of estrogens that are known to occur naturally within living organisms. In fact, isoflavones mediate numerous health effects mainly related to their estrogenic and/or anti-estrogenic actions. Some of these effects are estrogen receptormediated physiological phenomena such as those linked to the hypothalamo-hypophysogonadal axis. This book provides in vitro, animal, and clinical data intending to highlight the impact of isoflavones on the physio-cellular features of the hippocampal formation plasticity and, therefore, on the hippocampus-dependent cognitive brain function.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 64

MULTIPLE FACETS OF ANGER: GETTING MAD OR RESTORING JUSTICE? Farzaneh Pahlavan Université René Descartes, Cedex, France

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY This book examines the current state of research on anger and reflects the expanding understanding of how anger as an emotion interfaces with other aspects of psychological functioning, including behavior. It takes into account work by pioneers in this field as well as efforts by new investigators, all of which have to deal with the ambiguity and subjectivity of the construct by being clear about how they conceptualize it. This book provides a representative sampling of cutting-edge research and theory on anger.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 65

NEUROPLASTICITY FOLLOWING SKILL AND STRENGTH TRAINING Alan J. Pearce and Dawson J. Kidgell Victoria University, Melbourne, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The ability for the human motor cortex to change based on experience is now well accepted. Termed neuroplasticity, convincing evidence is available to challenge the long held view of a functionally stable neocortex that is unable to change. This book presents and discusses data which was collected using the technique of transcranial magnetic stimulation (TMS), as evidence of neuroplasticity following short and long term skill and strength training.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 66

NEUROPLASTICITY IN THE AUDITORY BRAINSTEM: FROM PHYSIOLOGY TO THE DRUG THERAPY Angelo Salami University of Genoa, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY It is now known that the brain is actually capable of changing and developing throughout a lifetime. Our mental capacity is astonishingly large, and our ability to process widely varied information and complex new experiences with relative ease can often be surprising. The brain‘s ability to act and react in ever-changing ways is known as neuroplasticity. Decades of research have now shown that these changes can profoundly alter the pattern of neuronal activation in response to experience. According to the theory of neuroplasticity, thinking, learning, acting and hearing can change both the brain's physical structure and functional organization according to the peripheral stimuli. This book reviews the latest knowledge on the neuroplasticity in the auditory brainstem: from physiology to the drug therapy.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 67

NEUROSCIENCE IN THE AGE OF COMPLEXITY Franco F. Orsucci University of Kent at Canterbury, England

Nicoletta Sala University of Italian Switzerland, Switzerland

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Neuroscience is the scientific study of the nervous system. Traditionally, neuroscience has been seen as a branch of biology. Nevertheless, it is currently an interdisciplinary science that involves other disciplines such as psychology, computer science, mathematics, physics, philosophy, and medicine. As a result, the scope of neuroscience has broadened to include different approaches used to study the molecular, developmental, structural, functional, evolutionary, computational, and medical aspects of the nervous system. This book discusses and presents research on a number of topics in the field of neuroscience, including mind force theory; neural resonance; circle mapping; the generalized spectrum of dimensions; and epileptiform activity in hippocampal neuronal networks.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 68

NEUROSCIENCES IN MUSIC PEDAGOGY Frances Rauscher Dept. of Psychology, Univ. of Wisconsin, Oshkosh, WI, US

Wilfried Gruhn Univ. of Music, Freiburg, Germany

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The theme of this book is how to transmit topical knowledge and recent findings in neurosciences to the needs of music educators. The authors offer a comprehensive view of neuromusical research and its potential applications to music learning. They take into consideration that (1) knowledge as such is not transferable; we cannot force children to learn or push synapses to grow. We can only provide a stimulating environment and environmental conditions that enhance and support learning, and (2) knowledge acquisition is governed by factors that are not fully under conscious control and can hardly be influenced externally. Nevertheless, children learn and are extremely curious and eager to learn. Their cortex is the organ where new experiences and knowledge are processed by interconnected neurons (mental representations) which become activated when a similar sensorial input is perceived. Since musicians have become a favoured model of brain plasticity in neurosciences, pedagogical expectations arose that education could benefit from music, and that neurosciences could underpin this assumption with solid and robust research data.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 69

SOCIETY, BEHAVIOUR AND EPILEPSY Jaya Pinikahana The Epilepsy Foundation of Victoria Australia

Christine Walker Chronic Illness Alliance, Victoria, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Although clinical, neurological, biological, psychiatric and even therapeutic aspects of epilepsy have been fairly consistently reviewed, relatively little is known about the psychosocial aspects of this condition. The psycho-social consequences of epilepsy are arguably often more severe than the severity of epilepsy. Studies show that social exclusion, fear, anxiety, stress, suicide, unemployment and homelessness among people with epilepsy are higher than the general population. Although there are no viable eclectic theories of biopsychosocial aspects of epilepsy, there are several current psychological and sociological perspectives of this disorder. This book fills a gap in the literature on the psycho-social context of epilepsy.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 70

SYMBIOTIC BIOFILMS AND BRAIN NEUROCHEMISTRY Alexander V. Oleskin, Vladimir I. Shishov and Kristina Malikina Moscow State University, Moscow, Russia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY An overwhelming majority of known species of microorganisms form biofilms, i.e. spatially and metabolically structured communities embedded in the extracellular biopolymer matrix. Biofilm development is a complex multi-stage process involving reversible and, at a later stage, irreversible attachment of microbial cells to the substrate surface. Development also involves matrix formation, three-dimensional structuring of the whole community including the formation of mushroom- or pillar-shaped structures and, finally, the degradation of the biofilm and the dispersion of the cells involved. This book examines these processes in the example of microorganisms that interact with the animal or human organisms, playing the roles of symbionts or pathogens.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 71

WORKING MEMORY IN INFANTS Jing Sun and Nicholas Buys Griffith University, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY This book examines working memory in preterm and full-term infants at eight months after the expected date of delivery. Although numerous studies have reported that the overall development of preterm infants is comparable to that of full-term infants at the same corrected age, it is unclear to what extent the development of specific cognitive abilities is affected by prematurity and/or other factors such as medical complications. As preterm infants have a high rate of learning difficulties, it is possible that factors associated with prematurity specifically affect the development of some regions of the brain associated with working memory.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 72

NEURAL SIGNAL ESTIMATION THROUGH TIME-RESOLVED FUNCTIONAL IMAGING C. W. Tyler and L. T. Likova Smith-Kettlewell Eye Research Institute, San Francisco, CA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The most effective method for localizing the effects of neural activation throughout the human brain is Functional Magnetic Resonance Imaging (fMRI). However, there is currently no method able to derive from the fMRI signal the particular neural signals underlying the measured BOLD waveforms. The goal of the present analysis is therefore to achieve timeresolved estimation of the neural signals determining the temporal waveforms in event-related fMRI. This analysis provides a new level of specificity in the basis of advanced approaches of using fMRI to study brain function as deep as at the level of the neural processing. In particular, we can resolve details of neural response dynamics down to the millisecond level for the analysis of visual processing and its temporal deficits. For this purpose, we develop a nonlinear dynamic forward model of the metabolic demand arising from the transmitter release in the minimal set of component neural populations that account for each fMRI waveform. This model allows derivation of the neural signals underlying the wide variety fMRI waveforms evoked from even the most elementary brief stimuli. Estimation of signal delays between cortical regions is enhanced by an autonormalization procedure to provide maximum temporal precision in mapping the causal interactions among functional subunits across the cortex by means of the pattern of simultaneous covariation in the fMRI responses. This technique is also robust to feedback processes, allowing the mapping of recursive feedback signal between cortical regions at different levels in the response hierarchy.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 73

DNA DAMAGE RESPONSE AND APOPTOSIS OF POSTMITOTIC NEURONS Inna I. Kruman1, and Elena I. Schwartz2 1

2

Sun Health Research Institute, Sun City, AZ, US Department of Pathology and Oncology, Georgetown University Medical Center, Washington, DC, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Programmed cell death or apoptosis is a relevant process in the physiology and pathology of the nervous system. Apoptosis is an organized form of cell death which is triggered by different factors including DNA damage. A growing body of evidence suggests that DNA damage and genomic instability are involved in neuronal abnormalities and may play a central role in neurodegeneration. DNA strand breaks and DNA lesions have been reported in Parkinson's and Alzheimer's diseases and as an early event after reperfusion of ischemic brain. DNA damage has been found to activate a cell death program in terminally differentiated postmitotic neurons. Since the genome is continuously damaged by a variety of endogenous and exogenous agents and the majority of DNA damage is produced by oxyradicals, generated by normal aerobic metabolism, neurons are particularly susceptible to DNA damage due to the high rate of oxidative metabolism. To maintain genomic integrity, cells are equipped with special defense mechanism, DNA damage response, to remove DNA damage by DNA repair pathways or eliminate damaged cells via apoptosis. Generally, differentiated cells, like neurons, are deficient in DNA repair and more vulnerable to DNA damage-initiated apoptosis. For example, neurons are more vulnerable than astrocytes to DNA-damaging conditions such as ionizing radiation. Breast cancer patients receiving hemotherapy commonly experience long-lasting cognitive impairment. It is known that radiotherapy may cause CNS toxicity. DNA damaging agents including γ-irradiation induce neuronal apoptosis in vitro, suggesting the direct adverse effect of these DNA damaging 

Correspondence concerning this article should be addressed to Correspondence to: Inna Kruman, Ph.D.; Sun Health Research Institute, 1015 West Santa Fe Drive, Sun City, AZ 85351; Tel.: 623-876-5607; FAX 623- 8765695; Email: [email protected].

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Inna I. Kruman and Elena I. Schwartz

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agents on neurons. The importance of DNA repair for neuronal survival is illustrated by disorders observed in patients with hereditary DNA repair abnormalities. These disorders combine the predisposition to cancer with progressive neurodegeneration. Although indirect evidence suggests that DNA damage and repair mechanisms play critical roles in neuronal survival, the pathways involved are poorly understood. Recently, we have found that cell cycle activation is essential for DNA damage-induced neuronal apoptosis which suggests that the cell cycle machinery is a critical element of the DNA damage response not only in cycling but also in quiescent cells. Here, we discuss the DNA damage response in postmitotic neurons and possible mechanisms by which neurons are forced to apoptosis versus DNA repair thereby controlling cell fate. Elucidation of these mechanisms promises to provide multiple points of therapeutic intervention in neurodegenerative diseases.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 74

HALLMARKS OF APOPTOTIC-LIKE CELL DEATH IN RESPONSE TO HYPOXIC INJURY IN VARIOUS DEVELOPMENTAL MODELS ARE CLOSELY RELATED TO BRAIN IMMATURITY Jean-Luc Daval1, and Christiane Charriaut-Marlangue2 1

INSERM U.724, Université Henri Poincaré, Faculté de Médecine, Vandoeuvre-lès-Nancy, France 2 Groupe Hypoxie et Ischémie du Cerveau en Développement, Université Pierre et Marie Curie-Paris, Paris, France

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY With regard to the specificity of the developing brain, a better understanding of cellular mechanisms involved in perinatal hypoxic-ischemic injury would help to prevent neurological impairments. We therefore examined temporal features of brain injury in three different developmental models of oxygen deprivation capable of inducing apoptotic cell death. Nuclear staining by DAPI (4,6-diamidino-2-phenylindole) was used to identify healthy, apoptotic and necrotic nuclei as well as for cell counting in cultures and brain sections. DNA fragmentation was monitored by in situ terminal dUTP nick end labeling (TUNEL) and electrophoresis on agarose gels. Also, the expression profile of apoptosis-related proteins Bax and Bcl-2 was studied by immunohistochemistry. In all cases, oxygen deprivation induced significant delayed cell death with morphological features of apoptosis and a progressive increase in the Bax/Bcl-2 protein ratio, except in the penumbra of the ischemic infarct where Bcl-2 remained predominant. As in the control newborn brain that still exhibited physiological death, hypoxia-associated DNA breakdown led to small fragments of ~200 bp in the cortex of hypoxic rat pups. Ladder pattern and TUNEL-positive cells exhibiting apoptotic bodies were only present in the penumbra of 7 day-old ischemic rats. 

Correspondence concerning this article should be addressed to Dr. Jean-Luc Daval, INSERM U.724, Université Henri Poincaré, Faculté de Médecine, 9 avenue de la Forêt de Haye, F-54500 Vandoeuvre-lès-Nancy, France. Email: [email protected].

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Jean-Luc Daval and Christiane Charriaut-Marlangue

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These data indicate that hallmarks of hypoxia-induced apoptosis may vary according to brain maturity, possibly through specific nuclease activities. While retaining a part of the developmental death program, the newborn brain seems to be prone to an apoptotic-like response that resembles physiological programmed death.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 75

THE USE OF NEURAL STEM CELLS IN TREATING TRAUMATIC BRAIN INJURY IN RATS Shu-Yuan Yang* and Hui Liu Department of Neurosurgery, Tianjin Medical University, General Hospital, Tianjin, People‘s Republic of China

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Objective: In this study we investigated the neuroprotective effect of transplants of Neural Stem Cells (NSCs) after experimental traumatic brain injury. Methods: NSCs were derived from human fetal hippocampi. The cells were injected into the cerebral cortex of rats subjected to experimental traumatic brain injury. The effect on the motor function scores of the rats was assessed. The techniques of immunohistochemistry and TUNEL were applied to define the NSCs‘ differentiation and neuroprotection. Results: Brain injured animals that received transplants of NSCs had marked and significantly improved motor scores compared with control groups. Animals that received NSCs transplants had significantly more surviving neurons compared with the vehicle treated brain injured rats. In situ TUNEL assay demonstrated fewer apoptotic cells in animals that received NSCs transplants than those of the control group. Conclusions: These results demonstrate the neuroprotective and functional efficacy of NSC transplants after experimental traumatic brain injury.

*

Address for reprints and correspondence: Professor Shu-Yuan Yang, M.D., Department of Neurosurgery, Tianjin Medical University, General Hospital, 154 An-Shan Road, Tianjin 300052, People‘s Republic of China. Phone: +86-22-6036-2621; Fax: +86-22-6036-2386; Email:[email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 76

SUBDURAL INTERICTAL EEG ANALYSIS FOR EXTRACTING DISCRIMINATING FEATURES TOWARDS ELECTRODE CLASSIFICATION USING ARTIFICIAL NEURAL NETWORKS Mercedes Cabrerizo*,1, Malek Adjouadi1, Melvin Ayala1 and Prasanna Jayakar2 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Department of Electrical & Computer Engineering, Florida International University, Miami, FL, US 2 Brain Institute, Miami Children‘s Hospital, Miami, FL, US

RESEARCH SUMMARY This study introduces an algorithm dedicated at discriminating between electrodes that lead to a seizure onset from those electrodes that do not, using interictal subdural EEG data. The significance of this study is in classifying among all of these channels, all containing interictal spikes that are asynchronous and independent of location, which are selected randomly, those channels that lead to seizure from those that do not with the purpose of focusing the attention on those electrodes during epileptogenic focus localization. The main epileptogenic focus is supposed to evolve from the tissue located at the channels that present interictal activity, but sometimes this is no the case. The purpose is to gain a better understanding of the dynamics of subdural EEG, while characterizing the common behaviors of interictal EEG channels prior to an ictal activity. The merits of this algorithm are: (a) its fast computational time and (b) its integrated signal processing design that identifies based on different parameters, electrodes leading or not to seizure. EEG signals were transformed into quantitative measures to account for those morphological characteristics of interictal signals deemed important in the classification process of channels leading or not to a seizure. *

Emails: [email protected], [email protected], [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 77

LABORATORY MEMORY TASKS AND AUTOBIOGRAPHICAL RECOLLECTION: COGNITIVE AND NEUROFUNCTIONAL EVIDENCE FOR DIFFERENTIAL FORMS OF EPISODIC MEMORY Martina Piefke

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Physiological Psychology, Department of Psychology and Sports Sciences, University of Bielefeld, Germany

RESEARCH SUMMARY The classic model of episodic memory refers to both laboratory tasks requiring the conscious recall or recognition of experimental materials and autobiographical recollection of one‘s personal past experiences. Recent research in cognitive neuroscience, however, showed evidence that laboratory and autobiographical memory may share aspects of conscious retrieval and reference to the temporal and spatial context at the time of encoding of information, but are different from each other in some important respects. The autobiographical memory domain is characterized by self-referential information processing, subjective emotional evaluation of memories, and the accompanying autonoetic conscious awareness. In contrast, laboratory episodic memory requires the effortful search for impersonal target information and the intentional use of retrieval strategies. Subregions of the prefrontal, medial temporal, and retrosplenial cortices appear to be differentially involved in the neural processing of each type of episodic memory, thus suggesting that they are supported by anatomically and functionally overlapping, but also segregated neural circuits.



Correspondence to: Martina Piefke, Physiological Psychology, Department of Psychology and Sports Sciences, University of Bielefeld, Universitätsstr. 25, 33615 Bielefeld, Germany. Tel.: ++49-521-106-4484. Fax: ++49521-106-6049. E-mail: [email protected].

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Martina Piefke

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The empirical data reviewed here support the view that laboratory and autobiographical episodic memory can at least in part be distinguished on the cognitive-behavioral and the neurofunctional levels. Accordingly, the review proposes an integrated view of laboratory and autobiographical forms of episodic memory which accounts for an overlap, but also emphasizes the unique features distinguishing the two memory types.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 78

BRAIN ELECTRIC SOURCE IMAGING BY AN ITERATIVE CORRELATION MATRIX BASED MULTIPLE SIGNAL CLASSIFICATION APPROACH Dezhong Yao Perception-Motor Interaction Laboratory, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, PR China

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY How to localize the neural electric activities effectively and precisely from the scalp EEG recordings is a critical issue for clinical neurology and cognitive neuroscience. In the 1980s and 1990s, suggested approaches included the dipole localization, cortical imaging, scalp Laplacian and 3D tomography. The 3D tomography may be realized by a direct linear inversion, or an indirect algorithm such as the subspace projection scanning method named MUltiple SIgnal Classification (MUSIC). However, the classical MUSIC algorithm is limited for its assumption of random noise. In this work, we propose to use a delay-correlation matrix instead of the previous zero-delay-correlation matrix in the signal-subspace estimate of the MUSIC algorithm to get a better performance over a spatial coherent but temporal random noisy disturbance. Then an Iterative application of the Delay-correlation MUSIC (IDM) is emphasized to derive a reasonable reconstruction of the multi-sources. The present simulation and empirical data experiment show that final promising results are obtained.



E-mail: [email protected], www.neuro.uestc.edu.cn.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 79

MAPPING OF BRAIN OPERATIONAL ARCHITECTONICS Andrew A. Fingelkurts* and Alexander A. Fingelkurts BM-SCIENCE Brain & Mind Technologies Research Centre, Espoo, Finland

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Recent neuroscience is lacking of consistent theory and methods for understanding the mechanisms through which the brain orchestrate the symphony of perceptions, thoughts and actions. The aim of this Chapter is to contribute to a better understanding of such mechanisms by establishing methodological foundations of the Operational Architectonics framework of brain and mind functioning. The theory we offer provides a framework for mapping and understanding important aspects of the brain mechanisms that constitute perception, cognition, and eventually consciousness.

*

Correspondence concerning this article should be addressed to Dr. Andrew A. Fingelkurts BM-SCIENCE Brain & Mind Technologies Research Centre, PO Box 77, FI-02601, Espoo, Finland. E-mail: [email protected]. Url: http://www.bm-science.com/team/fingelkurts.html.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 80

NEURAL MECHANISMS IN ANXIETY AND PANIC Marcus Lira Brandão* and Julia Maria dos Santos Laboratório de Psicobiologia, FFCLRP, Ribeirão Preto, SP, Brasil Instituto de Neurociências & Comportamento - INeC, Ribeirão Preto, SP, Brasil

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Depending on the nature of the aversive stimuli or threatening conditions different types of fear responses are elaborated in the brain. Conditioning procedures using light, tones and contexts used as conditioned stimuli associated to unconditioned stimuli of moderate intensity causes orientated and active forms of defense reaction. Organized and oriented defense reactions seem to be linked to anxiety. On the other hand, intense fear conditioning or past experience with stressful situations originate active but disorganized forms of defensive responses that ensures emotional states of different nature. The faulty performance of these animals in the fear-potentiated startle and contextual fear procedure show similarities with panic attacks in man. A sequential pattern of defense reaction made up of arousal, immobility, escape and an incapacitating immobility is also seen when the prey are exposed to potential, distal and proximal signals emitted by the approaching predator. Efforts have been made to characterize the neural circuits recruited in the organization of the defensive reactions during these conditions. The prefrontal cortex, hippocampus and ventral periaqueductal gray are mainly involved in the integration of anxiety-like responses whereas the dorsal periaqueductal gray constitutes the main neural substrates for the integration of aversive states related to panic. In this chapter we summarize the evidence linking the brain‘s defense systems to the *

Correspondence concerning this article should be addressed to M.L. Brandão Laboratory of Neuropsychopharmacology, FFCLRP, campus USP, av Bandeirantes 3900, 14049-901, Ribeirão Preto, SP, Brazil. FAX: 55 16 36024830; e-mail: [email protected].

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Marcus Lira Brandão and Julia Maria dos Santos

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concept of anxiety-panic. The neural substrates of aversion in the hypothalamus seem to be in the middle of these processes. As a working hypothesis, it is advanced that past experience with stressors may lead to an emotional shift from the neural circuits responsible for the production of the usual defensive responses to environmental stressful events in higher brain structures towards disturbed or maladaptive defense responses related to panic attacks in brainstem structures. Therefore, prior experience with stressor events may shift orientated, active and organized motor patterns of appropriate defensive behaviors in response to contextual aversive stimuli towards non-oriented, fragmentary and uncoordinated motor acts. With great probabilities the switch mechanisms for these processes are part of the neural substrates of defense located at the level of the amygdala and the hypothalamus.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 81

PHASE SYNCHRONIZATION AT DIFFERENT FREQUENCY BANDS INDUCED BY THE EMOTIONAL FILM STIMULI OF HAPPINESS, SADNESS AND FEAR Tommaso Costa, Elena Rognoni, Dario Galati and Manuella Crini Department of Psychology, University of Turin, Turni, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The neural large-scale dynamics and the connectivity pathways among spatially separated neural groups are conceived as a fundamental brain mechanism to integrate and process information. The new measures of nonlinear interdependencies applied to EEG recordings, such as phase synchronization, have been recently shown to be highly sensitive to detect the dynamical change underlying the brain functions. In the present chapter, the patterns of interdependency among different brain regions were investigated extracting the Synchronization Index (SI) from EEG response to different emotional and non-emotional film stimuli. The three basic emotions of happiness, fear and sadness were induced with the goal to investigate the synchronization patterns at different frequencies bands specifically associated with the valence dimension (positive vs. negative) and with the distinct basic emotional systems. The comparisons among the experimental conditions showed several significant SI changes. The results demonstrated an overall decrease of SI during emotional stimulation compared to neutral, indicating an increase of complexity in the cortical dynamics. Further differences were found among the specific emotions, involving a distinct couple of electrodes with topographical effects at the frequencies bands examined. During happiness, we found a large pattern of synchronization in the left frontal hemisphere, especially in delta and theta waves, while fear, compared to neutral stimuli, showed a higher right synchronization, especially in beta waves. Largely different SI patterns emerged in the comparisons between the two negative emotions of fear and sadness,

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224

Tommaso Costa, Elena Rognoni, Dario Galati et al.

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suggesting that the basic emotions are mediated by specific synchronized activity. The observed emotion-related SI change supports the view that coupling-decoupling patterns among the neural networks may be a relevant neural mechanism for the emotional processing and that SI nonlinear analysis may contribute to describe how the brain generates the emotion.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 82

COGNITIVE ASPECTS IN IDIOPATHIC EPILEPSY Sherifa A. Hamed Department of Neurology and Psychiatry, Assiut University Hospital, Assiut, Egypt

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Epilepsy is a common medical problem. Several studies suggest that idiopathic generalized or focal epilepsies can adversely affect mental development, cognition and behavior. Epileptic patients may experience reduced intelligence, attention, problems in memory, language and frontal executive functions. The exact mechanisms of epilepsy-related cognitive dysfunction are poorly understood. Cognitive deficits with epilepsy may be transient, persistent or progressive. Transient disruption of cognitive encoding processes may occur with paroxysmal focal or generalized epileptic discharges while epileptogenesis-related neuronal plasticity, reorganization, sprouting and impairment of cellular metabolism are fundamental determinants for progressive cognitive deterioration. Also antiepileptic drugs (AEDs) have differential, reversible and sometimes cumulative cognitive adverse consequences. AEDs not only reduce neuronal irritability but also may impair neuronal excitability, neurotransmitter release, enzymes and factors critical for information processing and memory. The present article serves as an overview of recent studies in cognition in adult and children patients with epilepsy. In this review, we will also discuss the known adverse mechanisms of epilepsy and AEDs on cognition.



Corresponding author: Sherifa Ahmed Hamed, P.O.Box 71516. Telephone: +2 088 2371820. Fax: +2 088 2333327, +2 088 2332278, e-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 83

COGNITIVE IMPAIRMENT IN CHILDREN WITH ADHD: DEVELOPING A NOVEL STANDARDISED SINGLE CASE DESIGN APPROACH TO ASSESSING STIMULANT MEDICATION RESPONSE Catherine Mollica, Paul Maruff and Alasdair Vance Department of Paediatrics, University of Melbourne, Murdoch Childrens Research Institute, Royal Children's Hospital, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Cognitive difficulties are now recognized as a major driver of functional impairment in children with ADHD. However, to date, clinicians remain less aware of feasible and appropriate statistical approaches to measure cognitive and behavioural change in their patients. This chapter presents a practical statistical decision making rule and then outlines a clinician-friendly study design for ascertaining stimulant medication response in children with ADHD.



Parkville, Melbourne VIC 3052, Phone: 61 3 9345-4666. Fax: 61 3 9345-6002. e-mail: [email protected].

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Chapter 84

NOVEL THERAPIES FOR ALZHEIMER'S DISEASE: POTENTIALLY DISEASE MODIFYING DRUGS Daniela Galimberti, Chiara Fenoglio and Elio Scarpini Dept. of Neurological Sciences, "Dino Ferrari" Center, University of Milan, Milan, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The two major neuropathologic hallmarks of Alzheimer‘s disease (AD) are extracellular Amyloid beta (A) plaques and intracellular neurofibrillary tangles (NFTs). Several additional pathogenic mechanisms likely play a role in the pathogenesis of the disease, including inflammation, oxidative damage, ion disregulation and cholesterol metabolism. A number of compounds have been developed, trying to interfere with the above mentioned altered mechanisms. Conversely to symptomatic drugs available to date, these new compounds are supposed to modify pathological steps leading to AD, thus acting on the evolution of the disease. Some of them are under clinical testing, others are in preclinical phases of development. In this chapter, the main pathogenic steps leading to neurodegeneration will be discussed, together with an update of potentially disease-modifying drugs under testing.



Corresponding Author: IRCCS Fondazione Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Phone ++ 39.2.55033847. Fax ++ 39.2.50320430. e-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 85

COGNITIVE INTERVENTIONS TO IMPROVE PREFRONTAL FUNCTIONS Yoshiyuki Tachibana, Yuko Akitsuki and Ryuta Kawashima Department of Functional Brain Imaging, IDAC, Tohoku University, Sendai, Japan

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The human prefrontal cortex (PFC) plays major roles in higher cognitive functions necessary for maintaining a healthy social life. Psychological and psychiatric problems are often associated with cognitive impairments associated with PFC. Thus, previous cognitive intervention studies have been conducted to improve the functions associated with PFC. In this article, first we describe the functions associated with PFC and its importance in cognitive intervention studies. Then, we describe recent advancements in cognitive intervention methods, particularly interventions to prevent cognitive decline in healthy older adults and those to enhance their emotional control and resilience in preschool children. We also discuss on transfer effects of previous cognitive intervention, which are often observed. Finally, we discuss on the unresolved issues on the mechanism underlying the effect of cognitive intervention. We consider that a deeper understanding of the effect of cognitive intervention will greatly contribute to human welfare and education for all generations. Further multidisciplinary research will be required to achieve this ultimate goal.



Correspondence should be addressed to: Yoshiyuki Tachibana, Seiryo-machi 4-1, Aoba-ku Sendai, 980-8575, Japan. Tel/Fax: +81-022-217-7988. [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 86

INSIGHTS FROM PROTEOMICS INTO MILD COGNITIVE IMPAIRMENT, LIKELY THE EARLIEST STAGE OF ALZHEIMER’S DISEASE Renã A. Sowell1 and D. Allan Butterfield1,2,3 1

2

Department of Chemistry, University of Kentucky, Lexington, KY, US Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, US 3 Center of Membrane Sciences, University of Kentucky, Lexington, KY, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Mild cognitive impairment (MCI) is arguably the earliest form of Alzheimer‘s disease (AD). Better understanding of brain changes in MCI may lead to the identification of therapeutic targets to slow the progression of AD. Oxidative stress has been implicated as a mechanism associated with the pathogenesis of both MCI and AD. In particular, among other markers, there is evidence for an increase in the levels of protein oxidation and lipid peroxidation in the brains of subjects with MCI. Several proteins are oxidatively modified in MCI brain, and as a result individual protein dysfunction may be directly linked to these modifications (e.g., carbonylation, nitration, modification by HNE) and may be involved in MCI pathogenesis. Additionally, Concanavalin-A-mediated separation of brain proteins has recently led to the identification of key proteins in MCI and AD using proteomics methods. This chapter will summarize important findings from proteomics studies of MCI, which have provided insights into this cognitive disorder and have led to further understanding of potential mechanisms involved in the progression of AD.



Correspondence to: D. Allan Butterfield, University of Kentucky, Lexington, KY 40506-0055, USA. Ph: (859)257-3184. Fax: (859)-257-5876. e-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 87

ANIMAL MODELS FOR CEREBROVASCULAR IMPAIRMENT AND ITS RELEVANCE IN VASCULAR DEMENTIA Veronica Lifshitz and Dan Frenkel Department of Neurobiology, the George S Wise Faculty of Life Sciences, Tel-Aviv University, Tel Aviv, Israel

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Dementia is one of the most predominant neurological disorders in the elderly. The prevalence and incidence of degenerative diseases, such as Alzheimer’s disease (AD) and vascular dementia, strongly correlate with age. Vascular dementia (VaD) is recognized as the second most prevalent type of dementia and described as a multifaceted cognitive decline resulting from cerebrovascular injury to brain regions associated with memory, cognition, and behavior. Vascular risk factors including diabetes, insulin resistance, hypertension, heart disease, smoking and obesity are each independently associated with an increased risk of cognitive impairment and dementia. This review will summarize relevant animal models for studying cognitive deficits as well as diagnostic assessment of VaD in humans with the intention of developing both an early diagnostic capability and future therapeutic interventions.



Corresponding author: Dan Frenkel, Sherman building, Room 424 Tel Aviv, Israel 69978. Telephone: 972-36409484. Fax: 972-3-6409028. e-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 88

THE CRITICAL ROLE OF COGNITIVE FUNCTION IN THE EFFECTIVE SELF-ADMINISTRATION OF INHALER THERAPY S. C. Allen The Royal Bournemouth Hospital, Bournemouth, Dorset, UK

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The morbidity and mortality from asthma remain high in patients over the age of 75 years in developed countries, in contrast to the improving mortality from that condition in children and younger adults. One of the reasons for this might be the relatively poor performance with inhaler devices confirmed by surveys of technique in elderly patients. Also, it has been shown that the most prominent determinants of adequate inhaler technique in old age are global cognitive function, frontal executive function and ideo-motor praxis. This review explores the pattern of observed and measured errors in the use of various inhalers in old age. The cognitive barriers to a successful grasp of inhaler technique are explained. The review then proceeds to describe a systematic research sequence by the author and others to identify factors that determine the likelihood of an aged person being able reliably to self-administer medication by the inhaled route, also drawing on parallel evidence from studies of spirometry technique. Relatively simple tests of cognition, praxis and executive function are described which have been shown to have predictive value in assessing frail elderly subjects for potential inhaler therapy or spirometry. The evidence presented can enable clinicians, particularly geriatricians, internists and pulmonologists to approach inhaled therapy for asthma and chronic obstructive pulmonary disease in a logical and effective way for their frail elderly patients. Further, it will be argued that the relation between congitive function and inhaler technique can be seen as a clinical metaphor for other self-administered tests or treatments, such as insulin therapy. There is scope for research to determine the predictive role of cognitive function tests in a wide range of self-treatment settings, particularly for patients with relatively mild unrecognized cognitive impairment. 

E-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 89

FOETAL ALCOHOL SPECTRUM DISORDERS: THE 21ST CENTURY INTELLECTUAL DISABILITY Teresa Whitehurst Sunfield Research Institute, West Midlands, UK

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The pattern of childhood disability now facing practitioners and clinicians across the world is an ever changing landscape. Both educators and medical professionals are challenged to develop new skills and new practices in order to address the complex array of symptoms and behaviours presented to them by the children and families seeking their support. In stark contrast to the ‗traditional‘ range of intellectual disabilities, whose causes are known and researched, such as Fragile X Syndrome, Down‘s syndrome and autism spectrum disorders, practitioners are now faced with the challenge of ‗man-made‘ intellectual disabilities such as Foetal Alcohol Spectrum Disorders (FASD). Despite this disorder being regarded as the leading known cause of non-genetic intellectual disability in the Western World with prevalence rates estimated at 1 in 100 there is scant public awareness of the dangers of drinking whilst pregnant, insufficient or contradictory guidance on ‗safe‘ limits, little or no professional knowledge base and a paucity of strategies to support those affected or their families. In a culture which sees binge drinking on the increase, the numbers of children with FASD are set to escalate. To what extent are our professionals ready for the challenges of this 21st Century intellectual disability? This chapter considers the neurological deficits of those affected by FASD, the implications for education both as a proactive and reactive strategy, the importance of early diagnosis and intervention, set within a context of need.



Woodman Lane, Clent, Stourbridge, West Midlands, DY9 9PB, United Kingdom. Telephone: 01562 881320. Email: [email protected].

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 90

WHERE THERE ARE NO TESTS: A SYSTEMATIC APPROACH TO TEST ADAPTATION Penny Holding1, Amina Abubakar2 and Patricia Kitsao Wekulo3 1

Africa Mental Health Foundation, Kenya/ Case Western Reserve University, US 2 Tilburg University, Netherlands/ Utrecht University, Netherlands Kenya Medical Research Institute-Centre for Geographic Medicine Research Coast 3 Africa Mental Health Foundation, Kenya

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY In this chapter we outline a systematic approach to test adaptation developed through more than a decade of research in child development in both urban and rural settings in East Africa. Rationale: The literature on the use of psychological tests in diverse cultures is rich in examples that illustrate the necessity of making modifications to test content and administration techniques. The need to make modifications stems from fundamental differences in cultural experience between test takers in rural Africa and test takers in North America and Europe, for whom the majority of assessments have been designed. Without these modifications the psychometric qualities of the test data may be questionable and the distribution of scores elicited show a lack of sensitivity to within-population differences. Based upon the premise that no instrument can claim to be culture-free the appropriateness of an instrument to a specific target population needs to be determined by evaluating its psychometric properties in context, as well as its cultural, developmental and health or educational relevance. The Special Case of Test Administrators: Beyond the characteristics of the test taker, those developing tests need also to consider the expertise of the potential test administrators. Few countries in Africa posses a psychological service, and therefore also lack training opportunities in test administration and interpretation. It is preferable to use test

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Penny Holding, Amina Abubakar and Patricia Kitsao Wekulo

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administrators who are more familiar to the client group and are fluent in the local languages to expert strangers who are unable to understand the child‘s responses. Research studies in resource-limited settings are therefore likely to be dependent upon technicians with limited experience to administer their test batteries. This lack of experience needs to be taken into account in both test selection and the design of test instructions.

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Chapter 91

PAID PERSONAL ASSISTANCE FOR OLDER ADULTS WITH COGNITIVE IMPAIRMENT LIVING AT HOME: CURRENT CONCERNS AND CHALLENGES FOR THE FUTURE Claudio Bilotta, Luigi Bergamaschini, Paola Nicolini and Carlo Vergani

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Department of Internal Medicine, Geriatric Medicine Unit, Fondazione Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena IRCCS; University of Milan, Milan, Italy

RESEARCH SUMMARY Quality indicators recommend a comprehensive support for informal caregivers of elders with cognitive impairment in order to delay nursing home placement of care recipients, since care comes at high financial, psychological and physical costs for the caregivers. However, according to a recent European survey caregivers often have to pay for home support services, which can be afforded only by about one out of every three people with dementia. In the last two decades both the workforce providing non-institutional personal assistance and the funding for such services have dramatically increased. Also, over the next twenty years the population aged 50 to 75, which represents the main source of family caregiving, is expected to decrease compared to the population aged 85 and older, which includes the main care recipients. Private caregiving will thus gain even more importance. Improved satisfaction with personal assistance and fewer unmet needs were reported after receiving consumerdirected services than after receiving agency-directed services. There are several concerns related to the actual provision of paid personal assistance. Hard work, stress and high risk of job burnout, low wage levels and limited health care 

Corresponding author: Claudio Bilotta, Geriatric Medicine Unit, via Pace 9, 20122 Milan, Italy. Phone number: (+39) 02 5503 5412. Fax number: (+39) 02 5501 7492. E-mail: [email protected].

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Claudio Bilotta, Luigi Bergamaschini, Paola Nicolini et al.

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benefits for personal assistance workers can explain high job turnover rates. High turnover itself leads to the potential for substandard care, especially when dealing with vulnerable elders with cognitive impairment. Dementia-specific training can support the provision of high-quality care and also increase job satisfaction for workers. However, concerns have risen about inadequate education and training of care workers. Few studies have analyzed the quality of paid personal care for older adults with disabilities living at home, none of them specifically considering people with cognitive impairment. So far, providing personal aides with adequate training and acceptable job and general living conditions appears to be one of the strongest promoters of a better quality of care, especially for older adults with cognitive impairment.

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Chapter 92

NEUROTOXICITY, AUTISM, AND COGNITIVE IMPAIRMENT Rebecca Cicha, Brett Holfeld and F. R. Ferraro University of North Dakota, ND, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Much research has been conducted in regard to identifying various etiological pathways of developmental disorders, particularly autism. The existing literature indicates potential roles of exposure to neurotoxic substances, including heavy metals and various synthetic chemicals, to the development and exacerbation of autistic symptoms. This paper will serve as a review of the relevant literature implicating environmental exposure to neurotoxic agents as a possible contributor to the development of autistic features.



Address all correspondence to: F. Richard Ferraro, Dept. Psychology - University of North Dakota, CorwinLarimore Rm. 215, 319 Harvard Street Stop 8380, Grand Forks, ND 58202-8380, 701-777-2414 (O), 701-7773454 (Fax), e-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 93

COMMON QUESTIONS AND ANSWERS TO DEEP BRAIN STIMULATION SURGERY Fernando Seijo1, Marco Alvarez-Vega1, Beatriz Lozano2, Fernando Fernández-González2, Elena Santamarta3 and Antonio Saíz3 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Functional Neurosurgery Unit, Neurosurgery Department, Hospital Universitario Central deAsturias, Oviedo, Spain 2 Clinical Neurophysiology Department. Hospital Universitario, Central deAsturias, Oviedo, Spain 3 Radiology Department. Hospital Universitario Central deAsturias, Oviedo, Spain

RESEARCH SUMMARY When a new technique is introduced, a certain period of time is required for it to be improved and adjusted. The success of functional stereotactic procedures depends on a variety of factors: patient selection, methodology of choice and localization of the target, and the experience of the neurosurgery team. The learning curve resulting from the neurosurgery team‘s acquired knowledge is also notable. After 12 years of working with deep brain stimulation (DBS), operating on over 200 patients and implanting more than 380 DBS electrodes for different illnesses, Parkinson´s disease, dystonia, tremor and Horton‘s headache, we believe that our experience may be useful to others who are starting out in functional stereotactic procedures.



Servicio de Neurocirugía,Hospital Universitario Central Hospital de Asturias,33006, Oviedo, Spain. Tfno: 00-3498510800- Ext. 38164 Fax: 00-34-985 273657,E-mail: [email protected]

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 94

DEEP BRAIN STIMULATION AND CORTICAL STIMULATION METHODS: A COMMENTARY ON ESTABLISHED APPLICATIONS AND EXPECTED DEVELOPMENTS Damianos E. Sakas and Ioannis G. Panourias Department of Neurosurgery, University of Athens Medical School, Evangelismos Hospital, Athens, Greece

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RESEARCH SUMMARY Over the last twenty years, deep brain stimulation (DBS) has been increasingly accepted as an effective alternative treatment to the selective lesioning methods previously used in stereotactic and functional neurosurgery. This method, based on its reversibility and adaptability, has currently been used for the alleviation of medically-refractory cases of movement disorders, epilepsy, pain, and psychiatric diseases. In the present commentary, data comparing DBS with other brain stimulation methods such as electrical cortical stimulation (CS) and transcranial magnetic stimulation (TMS) are analyzed and the perspectives of the field are outlined. Progress in the related fields of neuromodulation, functional neuroprosthetic surgery, neuroinformatics, neurocomputation, and developments in neuroengineering that are expected to refine, enhance and widen the therapeutic applications of DBS are also discussed.



Damianos E. Sakas, MD. Department of Neurosurgery, Evangelismos Hospital, 4 Marasli Street, 10676 Athens, Greece. Tel: +30 210 7201704 -5. Fax: +30 210 7249986. Email: [email protected].

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 95

CORTICAL STIMULATION VERSUS DEEP BRAIN STIMULATION IN NEUROLOGICAL AND PSYCHIATRIC DISORDERS: CURRENT STATE AND FUTURE PROSPECTS* Damianos E. Sakas† and Ioannis G. Panourias

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Department of Neurosurgery, University of Athens Medical School, Evangelismos Hospital, and P.S. Kokkalis Hellenic Center for Neurosurgical Research, Athens, Greece

RESEARCH SUMMARY Therapeutic brain stimulation can be applied: a) in networks which are located in cortical and subcortical layers, b) in deep nuclei groups (relay nodes) or c) in combination. CS and DBS belong to the domain of operative neuromodulation and particularly to the field of neural networks surgery, defined as the field that studies and applies advancements in neural networks research, digitized stereotactic brain imaging and implantable electrical or electronic devices in order to alter electrically the signal transmission in the nervous system, modulate neural networks and produce therapeutic effects. Therapeutic brain stimulation methods are currently distinguished into two major categories: a) noninvasive and b) invasive. The noninvasive methods (rTMS, tDCS) stimulate electrically the brain cortex after applying electrical currents on the human scalp.

*



A version of this chapter was also published in Text of Therapentic Cortical Stimulation, edited by Sergio Canavero published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research. Correspondence concerning this article should be addressed to Dr. Damianos E. Sakas, MD. E-mail: [email protected].

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Damianos E. Sakas and Ioannis G. Panourias

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The invasive methods require the surgical implantation of specially designed electrodes either in contact with the cortex of the brain, i.e., CS, or in deeply located selected targets, i.e., DBS. Instead of ―invasive‖, the terms implantable or by implantable devices‖ are much more appropriate, as they do not carry the negative association of a traumatic intervention that is implied by the term invasive CS. In this chapter, we describe and compare the current state and future prospects of DBS and CS in the fields of neurology and psychiatry.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 96

INVASIVE CORTICAL STIMULATION FOR PARKINSON’S DISEASE AND MOVEMENT DISORDERS* B. Cioni†, A. R. Bentivoglio, C. De Simone, A. Fasano, C. Piano, D. Policicchio, V. Perotti and M. Meglio Functional Neurosurgery, Anesthesiology, and Neurology, Università Cattolica, Roma, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Ever since the observation that motor cortex (MI) stimulation (MI ECS) could relieve some patients suffering post-stroke movement disorders and, above all, the successful introduction of MI ECS for the treatment of Parkinson‘s disease by Canavero in 1998, extradural MI ECS has been employed for the treatment of several movement disorders. This chapter reviews this field.

*



A version of this chapter was also published in Text of Therapentic Cortical Stimulation, edited by B. Cioni published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research. Correspondence concerning this article should be addressed to: Dr. Beatrice Cioni, MD.E-mail: [email protected]

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 97

DEEP BRAIN STIMULATION IN EPILEPSY: EXPERIMENTAL AND CLINICAL DATA *

M. Langlois1, S. Saillet1, B. Feddersen5, L. Minotti1,2, L. Vercueil1,2, S Chabardès1 3, O. David1, A. Depaulis1, P. Kahane1,2,4 and C. Deransart†,1,2 1

Grenoble Institut des Neurosciences, INSERM U836-UJF-CEA, Neurology Department, and 3Neurosurgery Department, Grenoble University Hospital, 4Institute for Children and adolescents with epilepsy – IDEE, Hospices Civils de Lyon, France 5 Department of Neurology, Klinikum Grosshadern, University of Munich, Germany

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2

RESEARCH SUMMARY About 30% of epileptic patients do not respond to antiepileptic drugs, of whom only a minority can benefit from resective surgery. Such a therapeutic option is considered only in patients who suffer from focal seizures with an epileptogenic zone clearly identified and safely removable. Therefore, patients with seizures arising from eloquent cortices, or which are multifocal, bilateral, or generalized, represent a particular challenge to ―new‖ or ―alternative‖ therapies. For these patients, neurostimulation appears with a great potential. Different approaches to neurostimulation in epileptic patients now exist and depend on (i) the brain region which is targeted and (ii) the way the stimulation is applied. The aim of neurostimulation in epilepsy is to reduce the probability of seizure occurrence and/or propagation, either by manipulating remote control systems (vagus nerve stimulation, deep brain stimulation), or by interfering with the epileptogenic zone itself (repetitive transcranial magnetic stimulation, cortical stimulation). *

A version of this chapter was also published in Recent Breakthroughs in Basal ganglia Research, edited by Erwan Bezard published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research. † Corresponding author: Colin Deransart, Grenoble - Institut des Neurosciences, Centre de recherche Inserm U 836UJF-CEA-CHU, Equipe 9: Dynamique des Réseaux Synchrones Epileptiques, Université Joseph Fourier Faculté de Médecine, Domaine de la Merci, 38700 La Tronche, [email protected].

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256

M. Langlois, S. Saillet, B. Feddersen et al.

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In most cases, stimulation is delivered continuously or intermittently according to a scheduled protocol. In particular, new progress in biotechnology and EEG signal analysis now allows stimulation in response to detection of electrographic seizures (e.g., closed-loop stimulation). Here, we review the various experimental and clinical attempts that have been made to control epileptic seizures by the means of deep brain electrical stimulation.

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Chapter 98

PSYCHOSURGERY OF OBSESSIVE-COMPULSIVE DISORDER: A NEW INDICATION FOR DEEP BRAIN STIMULATION?

*

Dominique Guehl, Abdelhamid Benazzouz, Bernard Bioulac, Pierre Burbaud Service de Neurophysiologie Clinique, Université Victor Segalen Bordeaux 2, Place Amélie-Raba Léon, Bordeaux, France

Emmanuel Cuny, Alain Rougier Service de Neurochirurgie, Université Victor Segalen Bordeaux 2, Centre Hospitalier Pellegrin, Bordeaux, France

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Jean Tignol Service de Psychiatrie d‘Adultes, Université Victor Segalen Bordeaux 2, Centre Hospitalier Charles Perrens, Centre Carreire, Bordeaux, France

Bruno Aouizerate Service de Psychiatrie d‘Adultes, Université Victor Segalen Bordeaux 2, Centre Hospitalier Charles Perrens, Centre Carreire, Bordeaux, France Service de Neurophysiologie Clinique, Université Victor Segalen Bordeaux 2, Centre Hospitalier Pellegrin, Bordeaux, France

RESEARCH SUMMARY Obsessive-compulsive disorder (OCD) is a relatively common psychiatric condition with an estimated lifetime prevalence of 2–3% of the general population. It is generally characterized by a chronic course leading to a profound impairment in psychosocial functioning and quality of life. *

A version of this chapter was also published in Recent Breakthroughs in Basal ganglia Research, edited by Erwan Bezard published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research.

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Dominique Guehl, Abdelhamid Benazzouz, Bernard Bioulac et al.

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Although its pathophysiology is still far from resolved, an ample body of literature suggests the role of overactivity in the frontal-subcortical loops originating in the orbitofrontal cortex and the anterior cingulate cortex, respectively. Today, the wellestablished efficacy of antidepressants, acting preferentially by blocking serotonin reuptake, in addition to psychological treatments, have considerably changed the poor prognosis of the illness. However, both conventional therapeutic approaches failed to substantially alleviate obsessive-compulsive symptoms in 20–30% of cases. From these considerations, several surgical strategies have been successfully proposed for treating the resistant forms of OCD, including anterior capsulotomy, anterior cingulotomy, subcaudate tractotomy and limbic leucotomy. They have been performed in order to interrupt the orbitofrontal and anterior cingulate loops at either cortical or subcortical level, which have been found as disrupted in OCD. Despite these lesion-producing techniques have relatively low incidence of serious complications or undesirable effects, deep brain stimulation, as a reversible procedure, has recently been introduced in the field of OCD, primarily targeting the limb part of the internal capsule or the ventral caudate nucleus. It has been shown to be of promising benefit that should be considered with caution and confirmed by further research in this area.

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Chapter 99

DEEP BRAIN STIMULATION IN ADULT AND PEDIATRIC DYSTONIA

*

Laura Cif1, Simone Hemm1, Nathalie Vayssiere1 and Philippe Coubes†,2 1

Research Group on Movement Disorders, Department of Neurosurgery 2 Montpellier University Hospital, Montpellier, France

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY In numerous medical conditions, abnormal movements (dystonia, dyskinesia, myoclonus and tremor) are present, isolated or associated to other neurological deficits. Deep brain stimulation has been validated as a safe and efficient neurosurgical procedure in treating Parkinson‘s disease and essential tremor. Following the experience with ablative surgery for dystonia and high frequency stimulation for Parkinson‘s disease, chronic electrical stimulation of the internal globus pallidus (GPi) has been proposed to treat dystonic syndromes. Based on etiology and spread of symptoms, 82 patients were divided in subgroups separating, for each of them, children and adults: primary DYT1 dystonia, primary dystonia without DYT1 mutation, primary segmental dystonia, post anoxic cerebral palsy, pantothenate kinase associated neurodegeneration (PKAN) and mitochondrial diseases. Assessment was performed pre- and postoperatively by the Burke-Fahn‘s Marsden Dystonia Rating Scale, motor and disability sections. Bilateral electrode implantation was performed under general anaesthesia. High frequency (130 Hz), 450 microseconds pulse width and monopolar stimulation were used. Clinical improvement at three years was comparable for the groups of primary dystonia (82% for the motor scores) and for secondary dystonia and degenerative diseases, improvement was less important but still interesting (40%).

*

A version of this chapter was also published in Recent Reakthroughs in Basal ganglia Research, edited by Erwan Bezard published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research. † Correspondence should be addressed to Philippe Coubes: Tel/Fax: +33 (0) 4.67.33.74.64. E-mail address: [email protected] or [email protected].

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Laura Cif, Simone Hemm, Nathalie Vayssiere et al.

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The originality of the method consisted in the use of stereotactic MR imaging for the target selection without microelectrode recordings. This reduced the duration of the procedure and the risk of haemorrhage. Chronic high frequency stimulation of the GPi can be considered as an efficient and lasting treatment in primary dystonia and proposed in selected cases of secondary dystonia and degenerative disease.

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Chapter 100

DEEP BRAIN STIMULATION OF THE SUBTHALAMUS: NEUROPSYCHOLOGICAL EFFECTS

*

Rita Moretti, Paola Torre, Rodolfo M. Antonello and Antonio Bava1 1

Dip. Fisiologia e Patologia, Università di Trieste, Italy

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RESEARCH SUMMARY The basal ganglia were considered as a site for integrating diverse inputs from the entire cerebral cortex and funneling these influences via the ventrolateral thalamus to the motor cortex. The subthalamic nucleus (STN) has generally been considered as a rely station within frontal-subcortical motor control circuitry. The function of the STN in the current model of the basal ganglia organization was developed from animal model and neurodegenerative diseases with hypo- and hyperkinetic movement disorders: in this model, the STN represents a relay in the so-called ―indirect‖ pathway of the parallel basal ganglia-thalamocortical circuits. STN excitatory efferents reinforce the inhibition of basal ganglia output nuclei, the internal globus pallidus (GPi) and the reticular substantia nigra (SNr) on thalamo-frontal neurons. A ―direct‖ striato-pallidal pathway opposes the STN by normally inhibiting basal ganglia outflow, facilitating thalamo-frontal drive. Clinicians maintain firm conviction on the fundamental role of the basal ganglia, and of STN, in motor syndromes such as Parkinson Disease. Lesions at the level of STN lead to hemiballism and involuntary movements of the contralateral extremities.

*

A version of this chapter was also published in Basal Ganglia and Thalamus: Their Role in Congition and Behavior, edited by Rita Moretti published by Nova Science Publishers, Inc. It was submitted for appropriate modification in an effort to encourage wider dissemination of research.

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Chapter 101

SUBTHALAMIC HIGH-FREQUENCY DEEP BRAIN STIMULATION EVALUATED BY POSITRON EMISSION TOMOGRAPHY IN A PORCINE PARKINSON MODEL Mette S. Nielsen1, Flemming Andersen2, Paul Cumming2, Arne Møller2, Albert Gjedde2, Jens. C. Sørensen3 and Carsten R. Bjarkam1 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Department of Neurobiology, Institute of Anatomy, University of Aarhus, Denmark 2 PET Center, University Hospital of Aarhus, Denmark 3 Department of Neurosurgery, University Hospital of Aarhus, Denmark

RESEARCH SUMMARY Background: Subthalamic high-frequency deep brain stimulation (STN DBS) has during the last decade been widely used in the treatment of Parkinson‘s disease (PD) complicated by motor fluctuations and medicine-induced adverse effects. The exact mechanism of STN DBS is, however, still unelucidated. Objective: To evaluate whether STN DBS changes regional cerebral blood flow (rCBF) and oxygen consumption, by positron emission tomography (PET) in a non-primate large animal PD model of STN DBS. Methods: Three MPTP (1methyl-4-phenyl-1,2,3,6-tetrahydropyridine) intoxicated female Göttingen minipigs (age 8-12 months, weight 16-20 kg) were stereotaxically implanted unilaterally with a DBS electrode (Medtronic, model 3387) connected to a pulse generator (Medtronic, model 7424) placed subcutaneously in the neck region. Four to six weeks later the animals were anesthetized and placed in a PET scanner. Three water (H215O) and three oxygen (15O2) scans were performed, before stimulation with clinical parametres (continuous unipolar stimulation (electrode negative, case positive), amplitude 3V, frequency 160 Hz, and pulse-width 60 s) was initiated and followed by 5 water and oxygen scans 5, 30, 60, 120 and 240 min thereafter. 

Correspondence to: Mette Slot Nielsen. Department of Neurobiology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C, Denmark. Phone: (+45) 8942 3027. Fax: (+45) 8942 3060. E-mail: [email protected].

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264

Mette S. Nielsen, Flemming Andersen, Paul Cumming et al.

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The obtained data (the three baseline scans versus the five poststimulation scans) were analysed by parametric DOT-analysis after semiautomatic coregistration to an average MRI pig brain. Results: rCBF was significantly increased (t-value = 5.47, p-value < 0.05) at the electrode tip after initiation of stimulation, and non-significant increases of oxygen consumption occurred in the ipsilateral- (t-value = 3.67, p-value < 0.1), and contralateral cortex (t-value = 3.34, p-value < 0.1). Conclusion: Our results indicate that STN DBS increases local midbrain rCBF and oxygen consumption in centrally placed cortical areas. The minipig may thus be a well-suited animal model for further studies of the mechanism of STN DBS in PD.

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Chapter 102

CURRENT AND FUTURE PERSPECTIVES ON VAGUS NERVE STIMULATION IN TREATMENT-RESISTANT DEPRESSION Bernardo Dell’Osso, Giulia Camuri, Lucio Oldani and A. Carlo Altamura Department of Psychiatry, University of Milan, Milano, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Treatment-resistant depression (TRD) is a leading cause of disability and therapeutic strategies used for this prevalent and impairing condition include pharmacological augmentation strategies and brain stimulation techniques. Vagus nerve stimulation (VNS) is a brain stimulation intervention that has shown to decrease seizure frequency in partial-onset seizure patients. Subsequent trials performed on treatment-resistant patients with major depression indicated that VNS may be an effective and safe treatment. VNS involves minor surgery in which an electrode pair is wrapped around the left vagus nerve in the neck and connected to a generator implanted in the chest wall subcutaneously. Several methodological approaches have been employed in order to better understand the mechanism of action of VNS and its effects on neurobiological circuits involved in mood regulation. Despite its invasive nature, the tolerability profile of VNS seems to be favourable given that, differently from other brain stimulation interventions (i.e., ECT, rTMS, tDCS), VNS is a continuous and chronic stimulation. Even though previous positive results from clinical trials have led VNS to be approved by the FDA and the EMEA for the use in TRD, researchers are now focusing their efforts in the identification of possible predictors of response to VNS. Further investigation of the effects of VNS in the long-term treatment (>2 years) of TRD is also required.



Dr Bernardo Dell‘Osso, Department of Psychiatry, University of Milan, Fondazione IRCCS, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via Francesco Sforza 35, 20122 Milano, Italy. Phone: 02-55035994. Fax: 02-50320310.email:[email protected].

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Chapter 103

INTERHEMISPHERIC CONNECTIVITY: THE EVOLUTION AND NATURE OF THE CORPUS CALLOSUM Sarah B. Johnson and Manuel F. Casanova* Department of Psychiatry; University of Louisville, KY, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Though no one will doubt that animals have evolved into a shocking diversity of shapes and sizes, it is remarkable that the basic neurological layout of the vast majority of species, including at least all vertebrates and arthropods, remains preserved, with a pair of organs arranged about the longitudinal axis of the organism. Accordingly, Houzel and Milleret (1999) go on to suggest that this symmetric layout represents the manner in which we process and respond to our environment, with ―our senses basically proceed[ing] by a balance between pairs of sensors, as our acts result from a dynamic equilibrium between pairs of effectors, and our decisions often follow[ing] judgements from contrasting points of view‖. Though we perhaps perceive our surroundings in sensory pairs, it is imperative that the output efforts of our nervous system be united into a single, coherent, efficient response; as eloquently put by Charles Sherrington in 1906, ―the resultant singleness of action from moment to moment is a keystone in the construction of the individual whose unity it is the specific office of the nervous system to perfect‖. Based on this premise of a dichotomous receptive system requiring coherent processing and a coordinated response, ―the brain must be seen as an ensemble of several multiply interconnected neuronal systems, each with its own functional specialization, and integration must be seen as the process of interactive cooperation between these systems that allows efficient cognition and consistent behavioral control‖.

*

Contact Information: Manuel F. Casanova, MD; Department of Psychiatry; University of Louisville; 500 South Preston Street, Building A, Room 217; Louisville, KY 40202; Email: [email protected]; Tel: (502)8524077 (O).

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Chapter 104

WHITE MATTER LESIONS: FROM PRESENT TO FUTURE R. P. W. Rouhl1, R. J. van Oostenbrugge1,2 and J. Lodder1,2 1

Department of Neurology Cardiovascular Research Institute Maastricht (CARIM) Maastricht University Medical Centre, AZ Maastricht, The Netherlands 2

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RESEARCH SUMMARY White matter lesions are caused by cerebral small vessel disease, particularly by arteriolosclerosis. Arteriolosclerosis consists of a hyaline wall thickening with consequent narrowing of the arteriolar vessel lumen and tissue ischemia. Arteriolosclerosis relates to hypertension, and to other cerebral ischemic lesions (lacunar infarcts, symptomatic as well as asymptomatic). The instigating factors in the pathogenesis of arteriolosclerosis and therefore of white matter lesions, however, remain elusive. Most accepted of current theories is disruption of the blood brain barrier caused by endothelial dysfunction. New imaging modalities, like molecular imaging, and new insights in endothelial biology could therefore provide further insight into the pathogenesis of arteriolosclerosis. In the present chapter we will discuss these emerging issues, their potential pitfalls, and their possibility to eventually increase therapeutic options for the vascular pathology which underlies white matter lesions.

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Chapter 105

WHITE MATTER LESIONS AND AGING IN HIV INFECTION: IMPLICATIONS FOR DEVELOPMENT OF COGNITIVE DECLINE AND DEMENTIA Aaron M. McMurtray1, Beau Nakamoto1,2, Kalpana Kallianpur1 and Erin P. Saito3 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Department of Medicine, Neurology Division, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, US 2 Department of Neurology, Straub Clinics and Hospital, Honolulu, HI, US 3 Department of Native Hawaiian Health, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, US

RESEARCH SUMMARY The widespread availability of highly active anti-retroviral therapy has lead to long-term survival for many individuals living with HIV infection. With advancing age, many older individuals living with HIV infection are beginning to develop aging-related changes in the brain structure, including white matter lesions. Given the known effect of white matter lesions in the general population, these lesions are also likely to have important effects in aging HIVseropositive individuals as well. Aging related white matter lesions are considered to be structural manifestations of brain small vessel vascular disease. These lesions, more predominant in older individuals, are typically related to vascular risk factors such as hypertension and diabetes. Furthermore, the presence of white matter lesions is a known risk factor for development of cognitive decline and dementia. For example, when compared to normal elderly individuals, those with lacunar infarcts score lower on cognitive tests and have approximately twice the risk of developing dementia in the future. Additionally, lacunar infarction in certain ―strategic locations‖ such as the basal ganglia may result in profound cognitive deficits and even dementia. Multiple studies demonstrate that presence of leukoaraiosis is independently related to cognitive impairment in the elderly, and when present in patients with lacunar strokes, indicates increased severity of small vessel vascular

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Aaron M. McMurtray, Beau Nakamoto, Kalpana Kallianpur et al.

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disease and exacerbates adverse effects of these lesions on cognitive performance. In elderly individuals, cerebral manifestations of small vessel vascular disease are also important components of vascular dementia. The relationship between white matter hyperintensities and cognitive performance in HIV infection is an active area of ongoing research. Links between presence of white matter hyperintensities and worse performance on tests of psychomotor speed and verbal memory have been established. Other studies show that dementia in HIV infection is associated with decreased white matter volumes, indicating that in this population the loss of white matter may contribute to cognitive decline. Our own research demonstrates that white matter lesion volume in HIV infection is correlated with degree of cortical atrophy, a potential underlying substrate for cognitive decline and dementia. Other studies, however, have reported no relation between white matter lesions and cognitive performance in HIV infection. This discrepancy has been partially resolved with the advent of newer neuroimaging techniques, which allow improved detection of white matter injury and provide further evidence for a connection between white matter damage and the severity of cognitive impairment in HIVseropositive individuals. In conclusion, aging-related white matter hyperintensities likely contribute to development of cognitive decline and dementia in HIV infection, and physicians caring for HIV seropositive individuals should discuss the importance of treating vascular risk factors with their patients.

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Chapter 106

WHITE MATTER CHANGES IN DRUG ABUSE AND IN HIV-1 INFECTION Andreas Büttner1, Jeremias Wohlschaeger2, Ida C. Llenos3 and Serge Weis3 1

Institute of Forensic Pathology, University of Rostock, Germany 2 Institute of Pathology and Neuropathology, University Duisburg-Essen, Essen, Germany 3 Laboratory of Neuropathology, Department of Pathology and Neuropathology, State Neuropsychiatric Hospital Wagner-Jauregg, Linz, Austria

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RESEARCH SUMMARY White matter is composed of axons that arise from neurons located in the gray matter. The axons are wrapped by myelin sheaths that constitute extensions of oligodendroglial cell membranes. Due to the staining properties of the myelin sheaths, this region stains light on sections, hence the name ―white matter‖. In addition, astrocytes, microglia and vessels are found in the white matter. Due to its oval form on horizontal sections of the brain, the white matter of the telencephalon is called centrum semiovale. By blunt dissection, different fiber systems of the white matter become apparent. The fiber systems of the white matter are distinguished as follows: (1) projection fibers, (2) association fibers, and (3) commissural fibers.

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Chapter 107

WHITE MATTER CHANGES IN CRITICAL ILLNESS AND DELIRIUM Max L. Gunther*1 2,3, Carlos Faraco4, 5 and Alessandro Morandi1 6,7

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

1

Vanderbilt University Medical Center, Center for Health Services Research, TN, US 2 Vanderbilt University, Department of Radiological Sciences, Nashville, TN, US 3 Vanderbilt University Medical Center – VUIIS, Vanderbilt Institute of Imaging Sciences, TN, US 4 Paul D. Coverdell Neuroimaging Center, University of Georgia, GA, US 5 University of Georgia Department of Psychology, 6 Department of Internal Medicine and Geriatrics, GA, US Poliambulanza Hospital, Brescia, Italy 7 Geriatric Research Group, Brescia, Italy

RESEARCH SUMMARY In the United States alone, over 50,000 individuals are treated daily in intensive care units (ICUs). Approximately 50-80% of ICU patients develop delirium with over half of these cases leading to meaningful and permanent losses in brain functioning. This suggests that critical illness may lead to de novo long-term pathological changes in the central nervous system. In the current chapter we review the evidence regarding links between white matter changes related to critical illness. In particular, we focus on both acute and distal alterations in white matter that may be caused by a number of factors including severe infection, glial cell atrophy, declines in axonal fractional anisotropy (FA) and global hypoperfusion. Evidence from several areas of the neurosciences (animal models, neuroimaging, case studies, etc.) suggest that delirium may be a hallmark of more permanent changes that are occurring in the CNS.

*

All correspondence and reprint requests should be sent to: Max L. Gunther, PhD; Center for Health Services Research; 6100 Medical Center East; Nashville, TN 37232-8300; Phone: 615-936-1010; Fax: 615-936-1269; Email: [email protected]; Web: www.ICUdelirium.org.

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276

Max L. Gunther, Carlos Faraco and Alessandro Morandi

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Taken together, the current evidence suggests that critical illness may be linked to disruption of white matter tracts in the brain eventually leading to long-term deficits in cognitive functioning. The chapter concludes by highlighting several methodological challenges in investigating these hypotheses along with future directions within the field of delirium and critical illness neuroscience research.

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Chapter 108

WHITE MATTER INVOLVEMENT IN NEUROMUSCULAR DISORDERS Petr Vondracek1, Marketa Hermanova2, Kristina Vodickova*3, Lenka Fajkusova4, Eva Brichtová5 and Jarmila Skotakova6

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

1

Department of Pediatric Neurology, University Hospital and Masaryk University, Brno, Czech Republic 2 Department of Pathology, St.Anne´s Hospital and Masaryk University, Brno, Czech Republic 3 Department of Pediatric Ophthalmology, University Hospital and Masaryk University, Brno, Czech Republic 4 Center of Molecular Biology and Gene Therapy, University Hospital, Brno, Czech Republic 5 Department of Pediatric Neurosurgery, University Hospital and Masaryk University, Brno, Czech Republic 6 Department of Pediatric Radiology, University Hospital and Masaryk University, Brno, Czech Republic

RESEARCH SUMMARY The frequency of inherited neuromuscular disorders in the human population is estimated to be approximately 1:3,500 worldwide. In some of these disorders there is an association of the neuromuscular and central nervous system (CNS) involvement. The explanation could be in a faulty process of expression of genetic information into the structure of vital proteins, which play a key role in both muscle and brain functions. In these multiorgan disorders a muscular dystrophy or peripheral neuropathy can be combined with the white matter lesion, or other structural abnormalities of the brain, eye, and other organs, and this combination can result in a spectrum of unusual clinical phenotypes.

*

Correspondence to: P. Vondracek, MD, PhD, Department of Pediatric Neurology, University Hospital, Cernopolni 9, 625 00 Brno, Czech Republic. tel.: +420-5-3223 4934, e-mail: [email protected].

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278

Petr Vondracek, Marketa Hermanova, Kristina Vodickova et al.

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The central nervous system involvement can be found especially in congenital muscular dystrophies (CMD, MDC), myotonic dystrophy types 1 and 2 (DM1, DM2), mitochondrial encephalomyopathies, and some variants of Charcot-Marie-Tooth disease (CMT). Our research is focused on these important hereditary neuromuscular disorders with the white matter involvement in pediatric patients, especially children afflicted with various forms of congenital muscular dystrophies. We present most interesting and unusual case reports of our patients to demonstrate difficulties and pitfalls in the diagnostics of these rare disorders. The white matter lesion is a very important and valuable diagnostic sign, and also could have a serious impact on the management and prognosis of patients with neuromuscular disorders.

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Chapter 109

WHITE MATTER HYPERINTENSITIES IN PSYCHIATRIC DISORDERS AND THEIR ASSOCIATION WITH SUICIDE RISK Maurizio Pompili1,2, Gianluca Serafini,1 Silvia Rigucci1, Andrea Romano3, Marco Innamorati4, Antonio Del Casale1, Daniela Di Cosimo1, Roberto Tatarelli1 and David Lester5 Department of Psychiatry, Sant‘Andrea Hospital, Sapienza University of Rome, Italy 2 McLean Hospital – Harvard Medical School, Boston, MA, US 3 Department of Neuroscience, Division of Neuroradiology, Sant‘Andrea Hospital, Sapienza University of Rome, Italy 4 Università Europea di Roma, Italy 5 The Richard Stockton College of New Jersey, NJ, US

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1

RESEARCH SUMMARY Suicide is a major worldwide public health problem. Nearly one million lives are lost from suicide each year and between 3%-5% of adults make at least one suicide attempt at some point in their life. Despite intensive efforts, research has failed to find necessary and sufficient factors that indicate an increased likelihood for suicide, and effective prevention strategies have remained elusive, suggesting that our understanding of the interplay of factors that increase the risk of suicide remains incomplete. Furthermore, although a great deal of research has been published on socio-psychological factors affecting suicidal behaviour, the results lack sufficient specificity. In recent years, studies have indicated that up to 43% of the variability in suicidal behaviour can be explained by genetics. Thus, combining independent clinical and biological predictors may provide improved predictive models.

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Maurizio Pompili, Gianluca Serafini, Silvia Rigucci et al.

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A great deal of research analyzing the neurobiological basis of suicide has been published in the last few decades. For examples, many studies have identified abnormalities of the serotonergic system in suicidal individuals, particularly in the ventral prefrontal cortex, as well as several other possible abnormalities, such as reduction in messenger RNA and protein levels of cyclic adenosine monophosphate response element binding, CRE-DNA binding activity, and basal and cyclic adenosine monophosphate–stimulated protein kinase A activity, noradrenergic overactivity, alterations in the levels of endocannabinoid and in the density of the CB1 receptors, lower grey-matter cholesterol content, elevated cholecystokinin mRNA levels, expression of proteins involved in glial function, neurodegeneration and oxidative stress neuronal injury, and higher β-adrenergic receptor binding. In the last decade, researchers have pointed out how the brain‘s white matter is implicated in mental illnesses. The aim of the present chapter is to review research on the association among white matter hyperintensities (WMH) and suicide behaviour.

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Chapter 110

A QUANTITATIVE STUDY OF THE PATHOLOGICAL CHANGES IN THE CORTICAL WHITE MATTER IN VARIANT CREUTZFELDT-JAKOB DISEASE (VCJD) Richard A. Armstrong* Vision Sciences, Aston University, Birmingham, UK

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RESEARCH SUMMARY The objective of this study was to determine the degree of white matter pathology in the cerebral cortex in cases of variant Creutzfeldt-Jakob disease (vCJD) and to study the relationships between the white matter and grey matter pathologies. Hence, the pathological changes in cortical white matter were studied in individual gyri of the frontal, parietal, occipital, and temporal cortex in eleven cases of vCJD. Vacuolation (‗spongiform change‘), deposition of the disease form of prion protein (PrPsc) in the form of discrete PrP deposits, and gliosis were observed in the white matter of virtually all cortical regions studied. Mean density of the vacuoles in the white matter was greater in the parietal lobe compared with the frontal, occipital, and temporal lobes but there were fewer glial cells in the occipital lobe compared with the other cortical regions. In the white matter of the frontal cortex, vacuole density was negatively correlated with the density of both glial cell nuclei and the PrP deposits. In addition, the densities of glial cells and PrP deposits were positively correlated in the frontal and parietal cortex. In the white matter of the frontal cortex and inferior temporal gyrus, there was a negative correlation between the densities of the vacuoles and the number of surviving neurons in laminae V/VI of the adjacent grey matter. In addition, in the frontal cortex, vacuole density in the white matter was negatively correlated with the density of the diffuse PrP deposits in laminae II/III and V/VI of the adjacent grey matter.

*

Corresponding Author: Dr. R.A. Armstrong, Vision Sciences, Aston University, Birmingham, B4 7ET, UK. Tel 0121-359-3611. Fax 0121-333-4220, EMail: [email protected].

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Richard A. Armstrong

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The densities of PrP deposits in the white matter of the frontal cortex were positively correlated with the density of the diffuse PrP deposits in laminae II/III and V/V1 and with the number of surviving neurons in laminae V/V1. The data suggest that in the white matter in vCJD, gliosis is associated with the development of PrP deposits while the appearance of the vacuolation is a later development. In addition, neuronal loss and PrP deposition in the lower cortical laminae of the grey matter may be a consequence of axonal degeneration within the white matter.

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Chapter 111

PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY Endre Pál* Department of Neurology, University of Pécs, Hungary

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RESEARCH SUMMARY Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease of the central nervous system. It is caused by opportunistic infection by the JC virus, a human polyomavirus. The primary infection is common and usually remains asymptomatic. The virus resides in the kidney in a latent form and can be reactivated when the immune system becomes compromised. B cells may transmit the virus to oligodendrocytes in the brain. Destruction of oligodendrocytes results in progressive and multifocal central nervous system symptoms and the outcome is usually fatal. PML has been increasingly detected in patients with AIDS and other secondary immunodeficiency conditions, and it might develop in exceptional cases with primary immunodeficiencies. Efficient therapies have not been established for patients with PML. Antiviral agents, highly active antiretroviral treatment in AIDS, and immunotherapies might be beneficial in acquired and iatrogenic immunodeficiency. The associated conditions, assumed pathomechanism, clinical and neuropathological features and therapeutic possibilities are summarized.

*

[email protected]; Tel: +36-72-535-900; Fax:+36-72-535-911.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 112

REMYELINATION FAILURE IN MULTIPLE SCLEROSIS AND VULNERABILITY OF OLIGODENDROCYTES TO REPEATED INSULTS Catherine Fressinaud* Neurology Department, University Hospital, Angers, France

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RESEARCH SUMMARY Oligodendrocytes (OL) synthesize myelin sheaths that insulate axons, forming the main components of the central nervous system (CNS) white matter. The considerable importance of this structure is well underlined by the fact that its lesions occuring during Multiple Sclerosis (MS) result often in patients severe disability. Permanent neurological deficit relies on axonal lesions that are associated with demyelination, and the remyelination process is impaired, for yet unknown reasons. To get insight into these pathophysiological phenomenons we have analyzed the capability of OL to synthesize myelin in MS chronic lesions. A constant and pronounced decrease in the number of myelinated fibres per OL compared to the adjacent normal appearing white matter (NAWM) was observed. This suggests that, at the cellular level, OL are incapable of synthesizing an appropriate number of myelin sheaths. Thus, restricted metabolic capacities of OL could result in their failure to remyelinate a sufficient number of damaged fibres, and might represent an important mechanism in MS, since, conversely, the number of OL is less constantly decreased. This hypothesis was supported by two sets of experimental data in vivo, and in vitro. In vivo, rat corpus callosum demyelination by lysophosphatidyl choline (LPC) stereotaxic microinjection is followed by spontaneous remyelination, and this process is significantly accelerated by treatment with either platelet-derived growth factor (PDGF). As expected, given the known proliferative effect of these growth factors on OL progenitors, the number of *

Correspondence to: Dr Catherine Fressinaud, Neurology Department, University Hospital, 4 rue Larrey. F49933 Angers Cedex 9. France; E-mail: [email protected]; Phone: 33 (0)2 41 35 46 13; Fax: 33 (0)2 41 35 35 94.

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Catherine Fressinaud

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OL increased by 20% in NT-3 remyelinated lesions compared to animals receiving LPC only, and, more interestingly, the number of myelinated fibres per cell increased far more, up to 100%, compared to spontaneous remyelination. Thus, these results strengthen the hypothesis that a more efficient remyelination relies not only on the availability of a sufficient pool of myelinating OL, but also, individually, on an increased capability of OL to synthesize myelin sheaths in large amounts, and that this ability too might be partly lost in MS. Since MS often evolves on a remitting-relapsing pattern, the repetition of attacks could represent one of the main factors that account for the failure of OL to remyelinate adequately lesions; nevertheless, the consequences for OL of repeated insults were largely unknown. In order to mimic this schematically, we have constructed an in vitro paradigm in which OL from newborn rat brain, grown in pure cultures, were submitted to either a single exposure to LPC (2.10-5 M, 24 h), or to several LPC exposures, although for shorter periods and at lower concentration (0.5 10-5 M, 4 x 6 h). Indeed, OL were very susceptible to multiple attacks versus a single one (despite a similar total dose and duration of treatment), and in particular mature OL – which are the myelinating cells, and constitute the major part of the population of cells of the OL lineage in the adult CNS –. Mature OL might thus represent the principal target of relapses during MS. Taken together our results converge, and suggest that cells of the OL lineage are particularly vulnerable to multiple insults, which lead both to the death of numerous cells and to restricted capability to synthesize myelin by surviving OL. This defect could constitute one of the significant causes contributing to their failure to remyelinate axons in MS. Our data add to the accumulating scientific knowledge suggesting that early treatment and attempts to avoid relapses are needed for patients suffering from MS.

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Chapter 113

ENDOSCOPIC ANATOMY OF THE THECAL SAC USING A FLEXIBLE STEERABLE ENDOSCOPE Jan Peter Warnke Neurology Department, Paracelsus Clinic, Zwickau, Germany

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RESEARCH SUMMARY The use of minimal invasive methods and edoscopic procedures for diagnosis and treatment of certain pathologic entities involving the spina canal expands permanently. The sacral spinal canal as a place of such interventions is for a long time known. Thecaloscopy is the endoscopy of lumbar subarachnoid space performed through different approaches by using flexible endoscopes. The subject of this study was the measurement of certain anatomic diameters in the sacral spinal canal by using the lubosacral MRI studies of 25 patients.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 114

WHITE MATTER ABNORMALITIES IN THE DIABETIC-HYPERTENSIVE BRAIN Natalia Rincon1 and Cory Toth2 1

2

University of Calgary, Calgary, Alberta, Canada University of Calgary and Hotchkiss Brain Institute, Alberta, Canada

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RESEARCH SUMMARY White matter fills nearly half of the brain, but receives disproportionately less scientific attention when compared to grey matter. For the past century, neuroscientists have demonstrated little interest in white matter, thought to be simply insulation for the more important axonal pathways contained within. The importance of white matter in learning tasks, mastering and executing mental and physical activities, as well as perfecting mental and social skills has become clearer over the recent decades. Much of this realization has developed from the study of diseases predominantly affecting white matter, and therefore disrupting intraneural communication, such as with multiple sclerosis and the leukodystrophies. Two diseases that have reached epidemic status—diabetes and hypertension—also contribute to white matter disease. The mechanisms by which these two common disorders affect white matter remain under study and may share commonalities but also disparities. Interestingly, the human condition of white matter abnormalities in patients with diabetes and/or hypertension can be modeled in rodents, with the hope that this will lead to future understanding and management.

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 115

BRAIN TISSUE SEGMENTATION BASED ON MULTI-CHANNEL DIFFUSION TENSOR IMAGING DATA Tianming Liu1 and Stephen T. C. Wong2 1

Department of Computer Science and Bioimaging Research Center, the University of Georgia, Athens, GA, US 2 The Center for Biotechnology and Informatics, the Methodist Hospital Research Institute, Weill Medical College of Cornell University, Houston, TX, US

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RESEARCH SUMMARY Brain tissue segmentation has important applications in studying the structure and function of the brain. A number of methods based on structural MRI data have been proposed for the segmentation problem. In this chapter, we present a robust method for automated brain tissue segmentation based on the multiple-channel fusion in DTI (diffusion tensor imaging) space. Our method can be employed to define accurate tissue maps when dealing with fused structural and diffusion MRI data. This enables us to study the gray matter diffusivity in neurodegenerative and neurological diseases. When fusing structural and diffusion information, the imperfect alignment of structural MRI data, e.g., SPGR (Spoiled Gradient Echo) image, with DTI data results in the problem of heterogeneous voxels when the anatomic information in the structural data is applied to the DTI data. Under the problem of heterogeneous voxels, the measurements of the GM (Gray Matter) diffusivity based on the anatomic information in the SPGR image may fail to reveal the real diffusion in the GM. Specifically, following non-rigid co-registration using the UCLA AIR tools, the GM boundaries of SPGR image are crossing CSF of ADC image. Consequently, the GM voxels in the SPGR image correspond to CSF (Cerebrospinal Fluid) voxels in the ADC (Apparent Diffusion Coefficient) image. Such a problem can occur for a variety of reasons, including geometric distortion in DTI imaging, partial volume effect, reslicing and interpolation of DTI data, and errors in co-registration.

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Chapter 116

THREE-DIMENSIONAL MICROSTRUCTURAL ANALYSIS OF HUMAN BRAIN TISSUE BY USING SYNCHROTRON RADIATION MICROTOMOGRAPHS Ryuta Mizutani*1, Akihisa Takeuchi2, Kentaro Uesugi2, Susumu Takekoshi3, R. Yoshiyuki Osamura3 and Yoshio Suzuki2 1

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Department of Applied Biochemistry, School of Engineering, Tokai University, Hiratsuka, Kanagawa, Japan 2 Research and Utilization Division, Sayo, Hyogo, Japan 3 Department of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, Japan

RESEARCH SUMMARY Recent application of synchrotron radiation to high-resolution computed tomography has resolved three-dimensional structures at micrometer to submicrometer resolution, although little is known about the microstructure of soft tissues including white matter of human brain. This is because soft tissues are composed of light elements that give little contrast in a hard xray transmission image. In clinical diagnosis, luminal structures of a living body are visualized by using x-ray contrast media. These contrast media contain high atomic-number elements that absorb x-rays efficiently. We have recently shown that the neuronal structure of human brain can be visualized by contrasting neurons using the metal impregnation method. Here, we report x-ray microtomographic studies of human cerebral cortex stained with high atomic-number elements. Staining protocols were developed to visualize the threedimensional microstructure of white and gray matter of human brain tissues. Methods for embedding and mounting soft tissues for the microtomographic analysis are also described. The obtained three-dimensional images revealed the microstructures of white and gray matter, which are responsible for human brain functions. *

Corresponding author: [email protected]. Abbreviations: CT, computed tomography; high-Z, high atomic number.

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Chapter 117

ORIGIN AND FUNCTION OF AMOEBOID MICROGLIAI CELLS IN THE PERIVENTRICULAR WHITE MATTER IN THE DEVELOPING BRAIN C. Kaur* and E. A. Ling Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

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RESEARCH SUMMARY Microglial cells are mononuclear phagocytes present ubiquitously in the developing brain. In the white matter, they first appear as round cells called the ameboid microglia which differentiate into ramified forms with maturation. The amoeboid microglial cells (AMC) are present in large numbers in the periventricular white matter (peripheral to the lateral ventricles) in the developing brain where they are known to exert other functions besides their primary phagocytic function. Although various theories have been proposed regarding the origin of these cells such as mesodermal, neuroectodermal and monocytic, their origin is still a matter of debate. The macrophagic nature of these cells has been demonstrated by different methods such as electron microscopy and immunohistochemistry. Expression of major histocompatibility complex class I and II antigens on them, induced by lipopolysaccharide or interferon-γ, supports their involvement in immune functions. They are also known to release cytokines and chemokines such as tumor-necrosis factor-α, interleukin-1β and monocyte chemoattractant protein-1 in inflammatory and hypoxic-ischemic injuries which may contribute to death of immature oligodendrocytes in such conditions. Recent investigations have reported that AMC also express potassium channels (Kv1.2) and release glutamate, nitric oxide and reactive oxygen species under hypoxic conditions. This chapter will review the origin and function of AMC in the periventricular white matter in the developing brain under normal conditions and the role of these cells in hypoxic/ischemic conditions.

*

Corresponding author: E-mail: [email protected]; Fax: 65-67787643; Phone: 65-65163209.

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Chapter 118

DIFFUSION TENSOR IMAGING IS MORE SENSITIVE THAN CONVENTIONAL MAGNETIC RESONANCE IMAGING IN DEMONSTRATING WHITE MATTER ABNORMALITIES IN SUSAC'S SYNDROME Ilka Kleffner*,1, Michael Deppe†,1, Siawoosh Mohammadi1, Philip Van Damme2, Stefan Sunaert3, Wolfram Schwindt4, Jens Sommer1, Peter Young1 and E. B. Ringelstein1 1

Department of Neurology, University of Muenster, Muenster, Germany Department of Neurology, Catholic University of Leuven, Leuven, Belgium 3 Department of Radiology, Catholic University of Leuven, Herestraat, Belgium 4 Department of Clinical Radiology, University of Muenster, Muenster, Germany Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

2

RESEARCH SUMMARY Objective: Susac's syndrome is characterized by the triad of hearing loss, branch retinal artery occlusions, and encephalopathy with predominantly cognitive and psychiatric symptoms. Focal ischemic lesions in the corpus callosum detectable by conventional magnetic resonance imaging (MRI) are a characteristic feature of Susac's syndrome. They do not, however, fully explain the type and severity of the neuropsychological deficits. In this study, we tested the hypothesis that widespread tissue damage of otherwise normal-appearing white matter (NAWM) can be detected in Susac's syndrome when using diffusion tensor imaging (DTI). Methods: Three-dimensional fractional anisotropy (FA) maps were calculated from DTI data of five patients with Susac's syndrome and a group of 63 matched healthy controls.

*

Corresponding author: Dr. med. Ilka Kleffner; Department of Neurology; University of Muenster; AlbertSchweitzer-Str. 33; 48129 Muenster; Germany; phone office: +49-(0)251-8348222; e-mail: [email protected]. † The authors Ilka Kleffner and Michael Deppe contributed equally to this study. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Results: Voxel-based statistics of spatially normalized FA maps revealed highly significant widespread impairment of fiber integrity in all patients. Lesions were particularly located in the genu of the corpus callosum and in the frontotemporal connecting fascicles. Patients showed specifically reduced mean FA values in the region of interest outlining the genu. This was true even if the genu was not focally affected on conventional MRI. Interpretation: We conclude that DTI is much more sensitive than conventional MRI in demonstrating WM abnormalities in Susac's syndrome. FA reductions in NAWM of the genu of the corpus callosum seem to be disease-specific. Psychiatric symptoms and cognitive deficits of these patients are most likely caused by the disruption of the anatomical connectivity of the frontal lobes.

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Chapter 119

ORGANISATION OF THE NODE OF RANVIER IN MYELINATED CENTRAL AXONS James J. P. Alix Academic Foundation Programme, Department of Medicine, Imperial College, London, UK

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RESEARCH SUMMARY The organisation of the myelinated central axon into discrete domains is key to the function of the central nervous system. While most of the axolemma is covered by lipid rich myelin, areas known as nodes of Ranvier are exposed to the extracellular space. These specialised regions are enriched with the Na+ channels responsible for action potential conduction, which, due to the low capacitance of the internodal myelin sheath, can travel with remarkable speed along even the smallest of myelinated axons. Restricting current flow in this way also lessens the metabolic burden of electrical activity, permitting the development of extensive white matter tracts. Recent work has identified numerous other proteins present at nodes and adjacent areas. These include, for example, the scaffolding proteins ankyrinG and β IV spectrin at the node and members of contactin associated protein family in the paranodal and juxtaparanodal regions. The exact mechanisms by which such proteins are recruited to the appropriate axonal domains remain elusive, although myelinating oligodendroglia appear to play an important role. This review will describe what is currently known about the organisation of Ranvier‘s node and the myelinated central axon.

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Chapter 120

ORGANIZING PRINCIPLES OF PROJECTIONS OF THE LONG DESCENDING RETICULOSPINAL PATHWAYS AND THEIR TARGETS’ SPINAL COMMISSURAL NEURONS: WITH SPECIAL REFERENCE TO THE LOCOMOTOR FUNCTION Kiyoji Matsuyama*1,2,3 and Kaoru Takakusaki4

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1

Department of Occupational Therapy, Sapporo Medical University School of Health Sciences, Department of 2 Neuropsychiatry and 3 System Neuroscience, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo, Japan 4 Department of Physiology, Asahikawa Medical College School of Medicine, Asahikawa, Japan

RESEARCH SUMMARY The neural control of locomotion in vertebrates involves continuous interactions between various kinds of neural subsystems which are widely distributed throughout the central nervous system. Among these subsystems, the long descending reticulospinal pathways and their targets‘ spinal lamina VIII commissural neurons with axons projecting across the midline to the contralateral side form a continuous, anatomical system that is involved in the generation and coordination of left-right reciprocal and bilateral locomotor activities. To advance understanding of locomotor roles of this brainstem-spinal cord system, we performed a series of neural tracing studies using anterograde neural tracers to characterize the axonal morphology of reticulospinal neurons and lamina VIII commissural neurons in the cat, with the goal of revealing some of the organizing principles of their projections along their rostrocaudal extent in the spinal cord, including: the number and frequency of their axon *

Corresponding should be addressed to Dr. Kiyoji Matsuyama. Department of Occupational Therapy, Sapporo Medical University School of Health Sciences, South-1, West-17, Chuo-ku, Sapporo 060-8556, Japan. Tel.: +8111-611-2111 (ext. 2880); Fax: +81-11-611-2155; E-mail: [email protected].

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collaterals in the white matter, the patterns of their collateral arborizations in the gray matter, and the relationships between locations of the parent axons and their collateral termination areas. The reticulospinal pathways are morphologically heterogeneous, being composed of various types of in-parallel-descending axons, each of which has a commonality of the pattern of collateral termination along its rostrocaudal extent in the spinal cord. Commissural neurons can be classified into two major groups on the basis of their projections, viz. those that project primarily to laminae VIII-VII and those that project to the motor nuclei in lamina IX. These suggest that the reticulospinal pathways and their targets‘ commissural neurons as a whole comprise varying types of functional subunits, which may serve as the flexible optimal neural substrate essential for the generation and coordination of the bilateral locomotor rhythm in self-induced, goal-directed locomotion.

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Chapter 121

DIFFUSION TENSOR MRI DATA ACQUISITION METHODS FOR WHITE MATTER AND CLINICAL APPLICATIONS: NON ECHO-PLANAR IMAGING Masaaki Hori Department of Radiology, Toho University, Ota, Tokyo, Japan

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RESEARCH SUMMARY Among several techniques, single-shot echo-planar imaging has been a standard technique for diffusion-tensor MR imaging (DTI) of white matter because of its rapid acquisition time and high signal to noise ratio. However, inherent artifacts and distortions due to susceptibility often prevent the demonstration of normal structures and pathological changes in some situations. Recently some studies have reported that line scan and single-shot fast spin-echo (ssfse) techniques (non echo-planar imaging techniques) have been used for DTI and their advantages. The line scan, simple spin-echo based one, can have benefits for brain stem and spinal cord imaging because of insensitivity of magnetic field inhomogeneity. Ssfse technique also avoids the artifacts and is useful for the region with geometric distortion (i.e., temporal lobe, metals after neurosurgical operation). However, these non echo-planar techniques have some disadvantages and therefore, are not commonly used in many institutions. In this chapter, we review and illustrate the merits and limitations of non echo-planar imaging techniques for the DTI. Moreover, we discuss the current role and feasibility of the DTI for white matter studies in brain and spinal cord, i.e. quantitative analysis of apparent diffusion coefficient in patients with cervical myelopathy, including results from our experiments and clinical data.

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Chapter 122

THE DIMENSIONS OF THE SACRAL SPINAL CANAL IN THECALOSCOPY: A MORPHOMETRIC MRI STUDY S. Mourgela*1, A. Sakellaropoulos2, S. Anagnostopoulou3 and J. P. Warnke4 1

Neurosurgical Department, ―Agios Savas‖ Anticancer Institute, Athens, Greece 2 Division of PCCM, Endoscopy and Sleep Medicine, Athens, Greece 3 Department of Anatomy, Medical School, University of Athens, Greece 4 Neurosurgical Department, Paracelsus Clinic, Zwickau, Germany

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RESEARCH SUMMARY The use of minimal invasive methods and endoscopic procedures for diagnosis and treatment of certain pathologic entities involving the spinal canal expands permanently. The sacral spinal canal as a place of such interventions is for a long time known. Thecaloscopy is the endoscopy of lumbar subarachnoid space performed through different approaches by using flexible endoscopes. The subject of this study was the measurement of certain anatomic diameters in the sacral spinal canal by using the lumbosacral MRI studies of 25 patients with unclear pain symptoms, in order to estimate, from the pure anatomic point of view, the capability to perform thecaloscopy in this anatomical region. Since now anatomic morphometric data of the sacral region were delivered only from the cadaver specimens‘ sectioning performed in anatomic institutes during the 60‘s and 70‘s years. The parameters measured were: 1. the inclination of the lumbosacral angle, 2. the duralsack‘s end, 3. the length of all the sacral spinal processes 4. The length of the sacral spinal canal in its centre and 5. The width of the sacral hiatus. The results of the measurements were in detail presented and an evaluation of them concerning the applicability of flexible endoscopes in the sacral spinal canal was performed. *

Correspondance: S. Mourgela, M.D. Neurosurgeon; Vikatou 12 str. 11524 Athens, Greece; E-mail: [email protected].

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It was proven that the duralsack‘s end in 40% of the patients at the middle of the S2 vertebral body lies, an anatomical position, which through the sacral hiatus easy to access is. The length under the sacral spinal processes is smaller than the length of the sacral spinal canal in its centre, a fact that makes the manipulation of a flexible endoscope easier, if someone works straight under the spinal processes and has a smaller distance to run. Through the sacral hiatus the introduction of the flexible endoscope is by many patients possible because of its adequate width.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 123

COCAINE'S IMPACT ON AFFECT, ACTIVITY, AND REWARD ARE DOSE-DEPENDENTLY IMPACTED BY AGE: ADOLESCENT VERSUS ADULT EXPOSURE Brian M. Kelley, Candace E. Perry, Hillary A. Hershey and Adrianna L. Baird Bridgewater College, VA, US

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RESEARCH SUMMARY The purpose of the present study is to examine the impact of different doses of cocaine on three interrelated measures related to affective behaviors between adolescent and adult mice. In order to assess the range of affective and rewarding responses, measure of despair, activity, and reward were used. Such methods included the forced swim test (FST), motor activity (MA), and the conditioned place preference (CPP) tests, respectively. Cocaine was selected, in part, because of its robust psychostimulant properties, it use by millions of substance abusers worldwide, and its well understood mechanism of action. The results show that adolescents have an increased sensitivity to cocaine‘s ability to alleviate despair compared to adults in the forced swim test. The adolescents showed a decreased sensitivity to the drug in the motor activity and conditioned place preference tests. The clinical implications of this study support an enormous body of clinical research, which suggest that substance abuse in primarily initiated during adolescence and that it often co-occurs with affective disorders. This study may help explain some of the neurobiological underpinnings of these finding because cocaine was especially effective in reducing despair-related behavior in adolescence compared with adults, yet less effective in as an euphoric agent. This is the worst possible finding because it suggests that adolescence will find cocaine particularly effective in alleviating mood resulting in increased use; however, in order to achieve euphoria higher doses will be required. The combination of these effects place youth at a particular disadvantage compared with adults and, as such, places them at a greater risk for lifelong substance abuse problems.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 124

MEETING ADOLESCENTS WHERE THEY ARE, LITERALLY AND FIGURATIVELY: EMBRACING EMERGING PERSUASIVE TECHNOLOGIES FOR TOBACCO CESSATION TREATMENT Brian M. Kelley

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Chair and Associate Professor of Psychology, Bridgewater College, Bridgewater, VA, US

The use of nicotine containing products in the United States is epidemic. Together, the use of cigarettes, cigars, and smokeless tobacco make nicotine one of the most heavily used addictive drugs in the United States (CDC, 2000; National Center for Health Statistics, 2006; CDC, 2007). Reports have found that approximately 153 million people 12 years and older (73.3%) have tried cigarettes; 66 million (31.7%) have smoked cigarettes in the past year; and 60 million (28.6%) are current cigarette users, with the highest rates of smoking occurring in people 18-25 years of age. Similarly, estimates suggest that about 10 million Americans use smokeless tobacco, 3 million of which are under the age of 21 (CDC, 1990 and 2005; National Cancer Institute, 2006). The US Department of Health and Human Services (Office on Smoking Health, 1994) reported that among daily smoking adults, 91% tried their first cigarette and 77.0% became daily smokers before 20 years of age; the mean age people reported becoming daily smokers was 14.5 years. This report also indicated that among high school seniors, who have ever tried smokeless tobacco, 73% did so by the ninth grade. Worse yet, the prevalence of cigarette, cigar, and smokeless tobacco use among older teens have increased over the last decade, not just in the United States, but worldwide as well (The Global Youth Tobacco Survey Collaborative Group, Tobacco Control, 2002). For example, cigarette use alone, which peaked just a decade ago at 34.8% (CDC, 2000), is currently at 28% (Substance Abuse and Mental Health Services Administration, 2005; 2007; 2008). Consequently, every day more than 4,000 adolescents try their first cigarette with more than 2,000 becoming daily smokers (CDC, 1998, 2003; U.S. Dept of Health and

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Brian M. Kelley

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Human Services, 2004). These statistics are particularly disturbing when you take into account the considerable knowledge young people have concerning the adverse health consequences associated with tobacco use. Despite such knowledge, tobacco use continues to be the leading preventable cause of death in the United States (McGinnis and Foege, 1993; CDC, 2003, 2005), responsible for approximately 440,000 deaths each year (CDC, 1996, 2003, 2005), and has an annual estimated economical impact of nearly $200 billion (CDC, 2000, 2005, 2007; Rice, 1995).

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Chapter 125

AN EXPLORATION OF HUMAN SWALLOWING USING TRANSCRANIAL MAGNETIC STIMULATION AND OTHER NON-INVASIVE TECHNOLOGIES S. Mistry, E. Michou, V. Jayasekeran and S. Hamdy University of Manchester, Department of Gastrointestinal Sciences, Salford Royal NHS Foundation Trust, UK

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RESEARCH SUMMARY Swallowing problems (dysphagia) are common after brain injury, and can affect as many as 50% of patients in the period immediately after stroke. In some cases this can lead to serious morbidity, in particular malnutrition and pulmonary aspiration. Despite this, swallowing therapies remain controversial, with limited evidence base and little in the way of objective outcome measures providing scientific support for the observed changes. Moreover, swallowing can recover in some patients to a safe level within weeks making it an interesting model for understanding brain recovery and compensation (plasticity). A better understanding of these adaptive processes, seen during the spontaneous recovery phase, may help in developing therapeutic interventions capable of driving brain changes and encouraging the recovery process and is therefore, a key goal for clinical neuroscience research which warrants systematic investigation. In this paper, we review current knowledge and discuss some of the pioneering work conducted by researchers from the Department of Gastrointestinal Sciences at the University of Manchester over the last decade in the field of human swallowing. We provide insights as to how the cerebral control of swallowing can be studied non-invasively in the human brain using neuroimaging tools and neurostimulation techniques such as functional magnetic resonance imaging (fMRI) transcranial magnetic stimulation



University of Manchester, Department of Gastrointestinal Science (Clinical Sciences Building), Salford Royal NHS Foundation Trust, Manchester, M6 8HD. Tel: +44 161 206 4414. Fax: +44 161 206 4364, Email: [email protected].

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S. Mistry, E. Michou, V. Jayasekeran et al.

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(TMS), repetitive TMS (rTMS), paired associative stimulation (PAS) and transcranial direct current stimulation (tDCS). In addition, we describe how using these neurostimulation techniques to manipulate the brain‘s natural capacity to reorganise (cortical plasticity) after injury or in response to new stimuli is helping to develop novel therapies for the treatment of dysphagia and other motor disorders in humans.

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Chapter 126

TRANSCRANIAL MAGNETIC STIMULATION AND THE HUMAN NEUROMUSCULAR SYSTEM Marisa P. McGinley and Brian C. Clark Institute for Neuromusculoskeletal Research, Department of Biomedical Sciences at the Ohio University College of Osteopathic Medicine, OH, US

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RESEARCH SUMMARY Transcranial magnetic stimulation (TMS) has been in use for more than 20 years, and has grown exponentially in popularity over the past decade. While the use of TMS has expanded to the study of many systems and process during this time, the original application and perhaps one of the most common uses of TMS involves studying the human neuromuscular system. Single pulse TMS applied to the motor cortex excites pyramidal neurons transsynaptically and results in a measurable electromyographic response that can be used to study and evaluate the integrity and excitability of the corticospinal tract in humans. Additionally, recent advances in magnetic stimulation now allows for partitioning of cortical versus spinal excitability. For example, magnetic stimulation of the cervicomedullary junction results in single descending volleys that have a large monosynaptic component and can thus be used to examine motorneuron excitability in some muscles. Conversely, paired-pulse TMS can be used to assess intracortical facilitatory and inhibitory properties by combining a conditioning stimulus and a test stimulus at different interstimulus intervals. In this book chapter the methodological and technical aspects of these techniques will be discussed along with the physiologic underpinnings.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 127

RTMS TREATMENT OF DEPRESSION: CURRENT STATUS AND FUTURE DIRECTIONS Paul B. Fitzgerald Monash Alfred Psychiatry Research Centre, The Alfred and Monash University School of Psychology, Psychiatry and Psychological Medicine, Victoria, Australia

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RESEARCH SUMMARY Since the mid-1990s a large number of clinical trials have studied the use of repetitive transcranial magnetic stimulation (rTMS) as a potential treatment for patients with major depressive disorder. Most of these studies have focused on the use of high frequency stimulation applied to the left dorsolateral prefrontal cortex (DLPFC) and this form of rTMS appears to have clear antidepressant properties. It has begun to be used clinically in a number of countries and was approved by the FDA in the US in 2008. Despite this, there appears to be some limits on the overall efficacy of this form of rTMS and efforts continue to try and develop other alternatives. A number of other forms of rTMS have been evaluated in clinical trials. These include low frequency stimulation applied to the right prefrontal cortex, bilateral stimulation approaches and a number of novel forms of rTMS. Emerging evidence suggests that some of these forms of stimulation may be more effective than the standard approach. Modifications to the way in which rTMS is applied are also being investigated and appear to have the potential for enhancing response to treatment.



Monash Alfred Psychiatry Research Centre,The Alfred First Floor Old Baker Building, Commercial Rd Melbourne, 3004, Victoria, Australia, 3181, Ph: 61 3 9076 6552. Fax: 61 3 9076 6588, E-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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Chapter 128

ANIMAL MODELS OF ALZHEIMER DISEASE FOR TRANSLATIONAL RESEARCH: CURRENT AND FUTURE CONCEPTS Shuko Takeda1,2, Naoyuki Sato1,2, Hiromi Rakugi2 and Ryuichi Morishita1 1

Department of Clinical Gene Therapy, Graduate School of Medicine, Osaka University, Yamadaoka, Suita, Osaka, Japan 2 Department of Geriatric Medicine, Graduate School of Medicine, Osaka University, Yamada-oka, Suita, Osaka, Japan

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RESEARCH SUMMARY The rise in the incidence of Alzheimer disease (AD) has become a major public health concern in many industrialized countries, and considerable effort is being directed toward the development of novel treatments for this disease. Excellent animal models for specific human diseases are indispensable for drug discovery and translational research. Transgenic mouse models harboring gene mutations found in rare inherited forms of AD have significantly facilitated research on the pathogenesis of AD and have played a pivotal role in developing novel disease-modifying therapies for this disease. However, although these potentially promising strategies demonstrated a marked improvement in these transgenic animals, most of the major completed clinical trials have been disappointing. The failure of these recent clinical trials has called into question the utility and validity of these animal models in preclinical testing of new therapies. Thus, current AD transgenic mice have insufficient therapeutic predictive validity as animal models of human AD, and might reflect only a limited aspect of human disease pathogenesis. Furthermore, in preclinical studies using animal models, the possibility of species differences between humans and model animals is a critical problem that should be carefully 

Department of Clinical Gene Therapy, Osaka University, Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan. Tel: 81-6-6879-3406. Fax: 81-6-6879-3409. E-mail: [email protected].

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considered. Of note, sporadic AD might be a multifactorial disease, and many genetic and environmental factors may affect disease progression. Modification of current transgenic animal models with known non-genetic risk factors might be useful and make them better suited for preclinical studies. This review summarizes the utility and limitations of current animal models of AD and discusses new trends in these models and their role in future drug development.

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Chapter 129

ENHANCEMENT STRATEGIES FOR TMS EFFECTS IN TINNITUS TREATMENT Tobias Kleinjung1,2* and Berthold Langguth2,3 1

Department of Otorhinolaryngology, University of Regensburg, Germany 2 Interdisciplinary Tinnitus Center, University of Regensburg, Germany 3 Department of Psychiatry and Psychotherapy, University of Regensburg, Germany

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RESEARCH SUMMARY Tinnitus is defined as the perception of sound or noise in the absence of any external or internal acoustic stimulus. Tinnitus is a frequent disorder and difficult to treat. Tinnitus is related to changes of neural activity in the central auditory system, but also in non-auditory brain areas. Repetitive transcranial magnetic stimulation (rTMS) over the temporal or temporoparietal cortex has recently been introduced as a new treatment strategy for tinnitus. The technique has been applied in two different ways in tinnitus patients. Single sessions of high-frequency rTMS have been successfully used for transiently disrupting tinnitus perception, whereas the administration of low-frequency rTMS in repeated session has demonstrated longer lasting reduction of tinnitus complaints in several studies. Even if all available controlled studies have shown a beneficial effect for rTMS, the data are characterized by only moderate effect size and relatively high inter-individual variability. Whether rTMS will become a treatment option for routine use or not will depend on the success of optimization strategies. This chapter reviews different approaches for the enhancement of rTMS effects in tinnitus patients. The different strategies include the combined stimulation of non-auditory and auditory brain areas, the variation of stimulation frequencies and intensities as well as the comparison of different firing modes (burst vs. tonic stimulation).

*

Department of Otorhinolaryngology, University of Regensburg, Germany, Interdisciplinary Tinnitus Center, University of Regensburg, Germany. Franz Josef Strauss Allee 11, 93053 Regensburg, Phone: +49 9419449505. Fax: +49 9419449512, E-mail: [email protected].

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Tobias Kleinjung and Berthold Langguth

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Furthermore, available knowledge about predictors for treatment success is discussed. Another approach consists in combination of rTMS administration with pharmacological intervention. Until now only the combined stimulation of auditory and non-auditory brain has shown some promise as an enhancement strategy. Furthermore shorter tinnitus duration seems to be a valuable predictor for positive treatment outcome.

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Chapter 130

TINNITUS AND TRANSCRANIAL MAGNETIC STIMULATION (TMS) Berthold Langguth1,2,* and Tobias Kleinjung2,3 1

Department of Psychiatry and Psychotherapy, University of Regensburg, Germany 2 Interdisciplinary Tinnitus Center, University of Regensburg, Germany 3 Department of Otorhinolaryngology, University of Regensburg, Germany

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RESEARCH SUMMARY Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive method for applying electromagnetical fields to the brain. rTMS can disrupt ongoing neuronal activity but also induce alterations of neuronal excitability that outlast the stimulation period. Tinnitus is the perception of sound in the absence of an external or internal sound source. Tinnitus is related to alterations in neuronal function in central auditory pathways. By modulating the excitability of the auditory cortex rTMS can influence tinnitus perception. Single sessions of rTMS over the temporal or temporoparietal cortex have been successful in transiently reducing tinnitus perception. Repeated sessions of rTMS have reduced tinnitus complaints in a subgroup of patients lasting from several days to several months. However, effect sizes of rTMS in the treatment of tinnitus are only moderate and interindividual variability is high. Further research is needed before this technique can be recommended for routine clinical use.

*

Department of Psychiatry and Psychotherapy, University of Regensburg, Germany, Interdisciplinary Tinnitus Center, University of Regensburg, Germany, Universitätsstr. 84, 93053 Regensburg, Phone: +49 9419412099. Fax: +49 9419412025, E-mail: Berthold.Langguth @medbo.de.

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Chapter 131

MUSIC AND CONCEPTS Jérôme Daltrozzo,1 Jean Vion-Dury2,3 and Daniele Schön2 1

2

CNRS-UMR, Lyon, France Mediterranean Institute of Cognitive Neurosciences, CNRS, Marseille, France 3 Neurophysiology and Psychophysiology Unit, Sainte Marguerite Hospital, Marseille, France

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RESEARCH SUMMARY What does music convey to the mind that may possibly explain its powerful effect on human behavior? While it is already well known that music can convey emotions, there is little evidence that it can also communicate concepts. We will first describe the theoretical framework that needs to be taken into account when studying conceptual processing in music. We will then present recent results that have been interpreted as signs of conceptual processing in music: the effect of a sound or a musical context on the processing of a target word (and vice-versa) as well as a gating paradigm exploring the unfolding of familiarity in music listening. These results are of interest in the discussion of whether separate neuronal networks or general cognitive resources are at work in processing concepts issued from different domains (e.g., language and music). Moreover, they are relevant to musical memory and the issue of a musical mental lexicon and the representations it may contain.

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Chapter 132

MOLECULAR MECHANISMS INVOLVED IN THE PATHOGENESIS OF HUNTINGTON DISEASE Claudia Perandones1, Martín Radrizzani2 and Federico Eduardo Micheli3 1

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Movement Disorders and Parkinson´s Disease Program, Hospital de Clínicas, José de San Martín, University of Buenos Aires, National Administration of Laboratories and Institutes of Health, ANLIS, Dr. Carlos G. Malbrán, Buenos Aires, Argentina 2 Neuro and Molecular Cytogenetics Laboratory, School of Science and Technology, National University of San Martín, CONICET, Buenos Aires, Argentina 3 Department of Neurology, Movement Disorders and Parkinson´s Disease Program, Hospital de Clínicas, José de San Martín, University of Buenos Aires, Argentina

RESEARCH SUMMARY Huntington's disease (HD) is an autosomal-dominant, progressive neurodegenerative disorder with a distinct phenotype, including chorea, incoordination, cognitive decline, and behavioral difficulties. The underlying genetic defect responsible for the disease is the expansion of a CAG repeat in the gene coding for the HD protein, huntingtin (htt). This CAG repeat is an unstable triplet repeat DNA sequence, and its length inversely correlates with the age at onset of the disease. Expanded CAG repeats have been found in 8 other inherited neurodegenerative diseases. Despite its widespread distribution, mutant htt causes selective neurodegeneration, which occurs mainly and most prominently in the striatum and deeper layers of the cortex. Remarkable progress has been made since the discovery of HD gene in 1993. Animal models to study the disease process, unraveling the expression and function of wild-type and mutant huntingtin (htt) proteins in the central and peripheral nervous systems, and understanding expanded CAG repeat containing mutant htt protein interactions with CNS proteins in the disease process have been developed. Consequently, it has been concluded that htt may cause toxicity via a wide range of different mechanisms. The primary consequence of

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Claudia Perandones, Martín Radrizzani and Federico Eduardo Micheli

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the mutation is to confer a toxic gain of function on the mutant htt protein, and this may be modified by certain normal activities that are impaired by the mutation. It is likely that the toxicity of mutant htt is only revealed after a series of cleavage events leading to the production of N-terminal huntingtin fragment(s) containing the expanded polyglutamine tract. Although aggregation of the mutant protein is the hallmark of the disease, the role of aggregation is complex and the arguments for protective roles of inclusions are discussed. HD progression has been found to involve several pathomechanisms, including expanded CAG repeat protein interaction with other CNS proteins, transcriptional dysregulation, calcium dyshomeostasis, defective mitochondrial bioenergetics and abnormal vesicle trafficking. Notably, not all the effects of mutant htt are cell-autonomous, and it is possible for abnormalities in neighboring neurons and glia to also have an impact on connected cells. The present review focuses on HD, outlining the effects of mutant htt in the nucleus and cytoplasm as well as the role of cell-cell interactions in the HD pathology. The widespread expression and localization of mutant htt and its interactions with a variety of proteins suggest that mutant htt is engaged in multiple pathogenic pathways. A better understanding of these mechanisms will lead to the development of more effective therapeutic targets.

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Chapter 133

HUNTINGTIN INTERACTING PROTEINS: INVOLVEMENT IN DIVERSE MOLECULAR FUNCTIONS, BIOLOGICAL PROCESSES AND PATHWAYS Nitai P. Bhattacharyya*, Moumita Datta, Manisha Banerjee, Srijit Das and Saikat Mukhopadhyay Crystallography and Molecular Biology Division and Structural Genomics Section, Saha Institute of Nuclear Physics, Kolkata, India

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RESEARCH SUMMARY To gain insight into role of Huntingtin (HTT) interacting proteins in pathogenesis of Huntington‘s disease (HD), in the present review, using various databases and published data we analyzed 141 validated HTT interacting proteins out of 311 proteins identified as the interactors of HTT. Results revealed that (i) all 141 proteins express in brain, (ii) fifty three HTT interacting proteins are down regulated and 36 proteins are increased in caudate of HD patients (iii) 25 proteins preferentially interact with mutated HTT, 19 proteins have higher affinity towards wild type HTT and 33 proteins interact equally and (iv) 120 HTT interacting proteins interact with 1780 unique other proteins including 67 HTT interacting proteins and having 2998 interactions altogether. Altered expressions of HTT interacting proteins and their preferences for the wild type and mutated proteins are likely to alter the network of HTT interacting proteins in HD resulting in cellular dysfunctions observed in HD. Several interacting proteins are known to modulate HD pathogenesis in cell, animal models and HD patients.

*

Correspondence: Nitai P. Bhattacharyya, Ph.D; Professor, Crystallography and Molecular Biology Division and Structural Genomics Section; 1/AF Bidhan Nagar, Kolkata 700 064, India; e.mail: nitaipada.bhattacharya@ saha.ac.in; [email protected]; Telephone: 091 033 23375345, extension 1301; Fax: 091 033 23374637.

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Nitai P. Bhattacharyya, Moumita Datta, Manisha Banerjee et al.

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Significantly enriched HTT interacting proteins in various functional categories, biological processes and pathways compared to that coded by human genome indicates that these functions, processes and pathways are altered in HD. All these data presented and reviewed in this chapter indicate that in spite of being a monogenic disease, HD is quite complex at molecular level. Understanding the molecular interactions and diverse pathways these interacting proteins participate are expected to help in devising therapeutic strategies to combat this devastating disease.

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Chapter 134

DNA REPAIR AND HUNTINGTON'S DISEASE Fabio Coppedè* Department of Neuroscience, University of Pisa, Pisa, Italy

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RESEARCH SUMMARY Huntington's disease (HD) is a progressive neurodegenerative disorder resulting in cognitive impairment, choreiform movements and death which usually occurs 15-20 years after the onset of the symptoms. A CAG repeat expansion within exon 1 of the gene encoding for huntingtin (IT15) causes the disease. In the normal population the number of CAG repeats is maintained below 35, while in individuals affected by HD it ranges from 35 to more than 100, resulting in an expanded polyglutamine segment in the protein. HD age at onset is inversely correlated with the CAG repeat length; moreover the CAG repeat length seems to be related to the rate of progression of neurological symptoms and motor impairment. Somatic CAG repeat expansion in the huntingtin gene has been observed in several tissues of HD patients, but particularly in the striatum, the region most affected by the disease. An agedependent somatic CAG repeat expansions was also observed in tissues of HD transgenic mice. Recently, it was found that somatic CAG repeat expansion is induced by oxidative stress in cultured HD fibroblasts and occurs during the repair of oxidized base lesions, dependent on a single base excision repair (BER) enzyme, the DNA glycosylase OGG1 which specifically removes oxidized guanine (8-oxo-G) from the DNA. It was therefore hypothesized that an age-dependent increase in 8-oxo-G formation in post-mitotic neurons could induce a DNA damage response mediated by OGG1 and give rise to a CAG repeat expansion that likely contributes to the onset and the progression of the disease. Further studies confirmed that somatic expansion of the CAG repeat tract in the brain is associated with an earlier HD age at onset.

*

Corresponding author: Department of Neuroscience, University of Pisa, Via Roma 67, 56126 Pisa, ITALY., Current Address: Department of Human and Environmental Sciences, University of Pisa, Via S. Giuseppe 22, 56126 Pisa, ITALY. Phone: +39 050 2211028, E-mail: [email protected].

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Fabio Coppedè

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Preliminary results from our group suggest that a common OGG1 Ser326Cys polymorphism could contribute to CAG repeat number and disease age at onset. Several subsequent studies support a role for oxidative DNA damage and BER to somatic instability of CAG repeats. There is also evidence that another DNA repair pathway, the mismatch repair (MMR), is required for the active mutagenesis of expanded CAG repeats. Since MMR is required for the repair of mismatched adenine opposite to 8-oxo-G, it remains to be seen if both BER and MMR co-operate physically in the process of CAG repeat expansion.

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Chapter 135

PUTTING TOGETHER EVIDENCE AND EXPERIENCE: BEST CARE IN HUNTINGTON’S DISEASE Zinzi Paola1, Jacopini Gioia1, Frontali Marina2 and Bentivoglio and Anna Rita3 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Consiglio Nazionale delle Ricerche, Istituto di Scienze e Tecnologie della Cognizione Rome, Italy 2 Consiglio Nazionale delle Ricerche, Istituto di Neurobiologia e Medicina Molecolare, Rome, Italy 3 Università Cattolica del Sacro Cuore, Istituto di Neurologia, Rome, Italy

RESEARCH SUMMARY Huntington‘s Disease (HD) is a late onset autosomal dominant neurodegenerative disease leading to movement disorders, dementia and psychiatric manifestations. The management of these patients, for whom there is still no cure, has been for long time neglected by clinicians. The identification of HD mutation in 1993 has raised a new interest in research as well as in clinical field and experimental data on patients care have begun to heap up. Among pharmacological therapies, data have become available on management of motor disorders with different types of neuroleptics or other classes of drugs while for the treatment of psychiatric and parkinsonian symptoms the available evidence is not specific for HD. Among non pharmacological therapies, rehabilitation has recently provided good results supported by measurable outcomes. Although these advances in management are encouraging, HD poses so many problems on so many different levels, that the way to attain an evidence based best care is still long. In this chapter we provide some discussion as to the best care in HD as well as to some ethical problems posed by the disease. We take into consideration either the advances attained in the different types of therapies or the knowledge acquired outside an experimental setting, during many years clinical practice with HD patients.

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Chapter 136

ORAL HEALTH CARE FOR THE INDIVIDUAL WITH HUNTINGTON’S DISEASE Robert Rada Department of Oral Medicine and Diagnostic Sciences, University of Illinois College of Dentistry, Chicago, IL, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY With the many advances in medical care, the dentist will be quite likely to be asked to treat patients with special health care needs. The dentist may be asked to recommend preventive regimens to maintain good oral health or provide comprehensive treatment of advanced dental disease. The patient with Huntington‘s disease is but one example of the debilitating effects systemic disease can have upon the oral cavity. There are no direct adverse affects on the oral cavity due to Huntington‘s disease; however complications associated with the disease increase the risk for dental caries and periodontal disease. As Huntington‘s disease progress, the person‘s ability to cooperate will diminish as functional and cognitive abilities decline. This will require the development of realistic treatment plans and easily maintainable dental restorations. Caregivers will need to be involved throughout the process as oral complications are likely throughout this long and difficult disease. Huntington characterized the disease by a triad of symptoms to include gradual personality changes, dementia and choreiform movements. Other symptoms include dysarthria, disturbances of gait and oculomotor dysfunction. The dementia is characterized by forgetfulness, slowness of thought and altered personality with apathy or depression. The patient can also become moody, irritable and incapable of dealing with the routine details of life. Subtle personality changes often become apparent before any motor symptoms arise. These conditions can all play a role in maintaining a healthy mouth. The dentist is likely to be among the first to notice a deterioration in oral health status.

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Chapter 137

SUICIDAL IDEATION AND BEHAVIOUR IN HUNTINGTON’S DISEASE Tarja-Brita1 and Robins Wahlin2* 1

Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden and 2 The University of Queensland School of Medicine, Brisbane, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Huntington‘s Disease (HD) is an autosomal-dominant neuropsychiatric disorder characterized by irreversible physical and mental deterioration, personality change, mental disorder, and increased susceptibility to suicidal ideation and suicide. Typically the disease has a very long course to run before death. There is little that the affected or HD persons who find out their carrier status can do, although if they come early for genetic testing, they can make reproductive choices. If the diagnosis or the predictive information has little therapeutic value to the patient, especially if there is no family, one possible available action is planning of a suicide. Higher suicide rates are reported for HD patients compared to the general population. It is also well known that persons with HD have an increased propensity to psychiatric dysfunction and elevated rates of catastrophic social events. Furthermore, surveys of attitudes about likelihood of attempted suicide have indicated that 5-29% of at risk individuals would contemplate suicide if they received a result indicating a carrier status. The prevalence of suicide and suicide attempts is difficult to estimate because of methodological problems. Suicide rates of HD populations vary among countries, and they are affected by factors such as socio-economic status, age, sex, and prevalence of HD.

*

Address for communication:Tarja-Brita Robins Wahlin, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Novum plan 5, 141 86 Stockholm, Sweden. Tel. +46 8 5858 9397. Fax: +46 8 5858 5470, E-mail: [email protected].

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Tarja-Brita Robins Wahlin

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It appears that cases of suicide vary from 1.6% to 13.8% in HD populations. In this chapter, suicidal behaviour, psychological affect of predictive testing, suicidal ideation and behaviour before and after predictive testing, and depression in HD, are discussed. At present, the problems associated with suicidal ideation and suicide in HD populations, worldwide, are much the same as two decades ago. The need for counselling, using a well designed protocol, and the importance of focusing on suicide risk of participants in predictive testing programs is emphasized.

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Chapter 138

MAKING REPRODUCTIVE DECISIONS IN THE FACE OF A LATE-ONSET GENETIC DISORDER, HUNTINGTON’S DISEASE: AN EVALUATION OF NATURALISTIC DECISION-MAKING INITIATIVES 

Claudia Downing† Research Fellow, Centre for Family Research, University of Cambridge, Free School Lane, Cambridge, England, UK

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY This chapter makes two contributions to the psychology of decision making. It draws on empirical work to document how family members make and live with reproductive decisions as they become aware of their risk for a serious late-onset genetic disorder, Huntington‘s disease (HD). Decision-making involves negotiating two dimensions of reproductive risk – that for any child which might be born and the uncertainty that arises about the at-risk parent‘s ability to sustain a parenting role should he or she become symptomatic. A detailed account is given of how the model of responsibility was generated from their narratives. This model encapsulates what families find important when making reproductive decisions. It demonstrates that how people make decisions can become as important as what they decide. Examples are given to show how the model provides a framework for comparing how people deal with each dimension of risk, to compare different people‘s decision-making and to



A version of this chapter was also published in Psychology of Decision Making in Medicine and Health Care, edited by Thomas E. Lynch published by Nova Science Publishers, Inc. It was submitted for appropriate modifications in an effort to encourage wider dissemination of research. † Correspondence to: Centre for Family Research, University of Cambridge. Free School Lane, Cambridge, England CB2 3RF [email protected].

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Claudia Downing

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illuminate decision-making in the face of change. This includes how they address new options generated by recent developments in molecular genetics which can resolve uncertainty about, or avoid these risks. A detailed account is also given of the process of their decision-making. These findings are used to evaluate claims being made by naturalistic decision-making (NDM) initiatives to account for decision-making in the real world. An outline of this initiative prefaces the research findings. Beach‘s (1990) image theory, used to illustrate the NDM approach, emphasises the role that values play in forming, negotiating, implementing and living with decisions that arise in everyday lives. Participants‘ accounts support this claim - revealing how values such as responsibility become established and contribute to decisionmaking. This and other findings lend support to the NDM claims. The chapter concludes with suggestions about how the model might be used more generally to further our understanding of the psychology of decision-making in the face of risk.

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Chapter 139

THE CONTROL OF ADULT NEUROGENESIS BY THE MICROENVIRONMENT AND HOW THIS MAY BE ALTERED IN HUNTINGTON’S DISEASE Wendy Phillips*1,2 and Roger A. Barker1,2 1

Cambridge Centre for Brain Repair, E.D. Adrian Building, Forvie Site, Cambridge, England, UK 2 Department of Neurology, Addenbrooke‘s Hospital, Hills Road, Cambridge, England, UK

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Neurogenesis is the processes whereby newborn neurons are formed and occurs in mammals in adulthood in specialised areas, known as ‗neurogenic niches‘. The subventricular zone, and subgranular zone of the dentate gyrus of the hippocampus are such specialised neurogenic niches and newborn neurons formed here contribute to learning and memory, but neurogenesis may occur elsewhere in the brain to a more limited extent. The neurogenic niche is composed of specialised glial cells, basal lamina, ependymal cells, neurotransmitter complement and vasculature. Neurogenesis is a complex process, involving many different cell types, and several stages of neuronal maturation; and each component may be affected by many different microenvironmental perturbations. External perturbations, like seizures and lesions alter the microenvironment and in turn, alter neurogenesis. Chronic disease can also affect neurogenesis and the inherited neurodegenerative condition Huntington‘s disease may do so through an alteration of the microenvironment. We will use the example of Huntington‘s disease to explore how changes in the microenvironment might impact on neurogenesis and, thus identify potential therapeutic targets.

*

Corresponding author: Dr. Wendy Phillips, Cambridge Centre for Brain Repair, E.D. Adrian Building. Forvie Site, Cambridge, CB2 2PY. E-mail: [email protected]; Tel: +44 1223 331160; Fax: +44 1223 331174.

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Chapter 140

EMOTION’S EFFECTS ON ATTENTION AND MEMORY: RELEVANCE TO POSTTRAUMATIC STRESS DISORDER Katherine Mickley Steinmetz* and Elizabeth Kensinger Boston College Psychology Department, Chestnut Hill, MA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Out of all of the information that we experience, only a subset will become part of our memories. Attentional processes, engaged during an event‘s unfolding, are essential for allowing us to transform an experience into a memory, and emotion can critically modulate those attentional processes, increasing the likelihood that an emotional experience becomes part of our memory stores. This chapter reviews behavioral and neuroimaging evidence that has revealed effects of emotion on memory and attention in individuals with and without post-traumatic stress disorder (PTSD). First, we review how emotion influences the attentional processes that allow individuals with and without PTSD to transform experiences into a memory. Second, we focus on differences in the way emotional items are remembered in people with and without PTSD and how this may be linked to differences in attention at encoding. Third, we discuss current controversies regarding the uniqueness of traumatic memories in PTSD.

*

Corresponding author: Department of Psychology, Boston College, 140 Commonwealth Ave., Chestnut Hill, MA 02467, Fax: 617-552-0523

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Chapter 141

LIFE SKILLS INSTRUCTION IN A TIME OF ACCOUNTABILITY Beth Ackerman and Katherine Quigley Liberty University, School of Education, Lynchburg, VA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY The current legislation, No Child Left Behind, mandates that students with intellectual disabilities have access to core curriculum courses. This action research investigates a comprehensive life skills program, Life Centered Career Education (LCCE), being integrated into the curriculum of high school students with intellectual disabilities. The LCCE program was utilized to educate students on Personal-Social Skills, Daily Life skills, and Occupational lessons with an academic emphasis.

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Chapter 142

PRO-INFLAMMATORY CYTOKINES IN LEARNING AND MEMORY Amaicha Mara Depino Consejo Nacional de Investigaciones Cientificas y Tecnologicas, Conicet—Faculty of Exact and Natural Sciences, University of Buenos Aires, Buenos Aires, Argentina

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY In animals and in humans, cytokines are typically immune system molecules that help orchestrate the host responses to infection. Pro-inflammatory cytokines coordinate immune, physiological, metabolic and behavioral responses that are collectively termed the acute phase reaction. In addition to their role in immunoregulation of inflammatory processes, proinflammatory cytokines represent the major communication link between peripheral immunity and the central nervous system. Cytokines are known to play a role in the physiological and behavioral adjustments that occur during sickness, leading to ―sickness behavior‖. One of the most salient symptoms of the sickness behavior syndrome is alteration in learning and memory processes. Studies in animals have demonstrated that acute activation of pro-inflammatory cytokine signaling in the brain in response to peripheral immune activation is associated with deficits in hippocampal-dependent memory. Recent studies suggest that brain cytokines may also have some physiological roles in neural, neuroendocrine, and behavioral regulation in non-pathological situations. Cytokineinduced modulation of memory processes is a complex phenomenon, including both detrimental and beneficial effects, depending on the specific pro-inflammatory cytokine, its levels (particularly within the brain), and the particular condition that elicits the cytokine secretion. Some cytokines, e.g., Interleukin (IL)-1, have been shown to significantly influence memory consolidation. IL-1, IL-6 and tumor necrosis factor (TNF)- are the main cytokines involved in learning and memory modulation. These behavioral data are consistent with the impairing effect of enhanced cytokine signaling on hippocampal long-term potentiation. We will review the literature, including our own contribution, on human and animal model studies of the role of cytokines in learning and memory.

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Chapter 143

PERCEPTIONS OF FORGETFULNESS IN ADULTHOOD: DOES MEMORY KNOWLEDGE MATTER? Susan Brigman and Katie E. Cherry* Louisiana State University, LA, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY We examined the effects of age and knowledge of memory aging on subjective appraisals of memory in forgetful others using a person perception paradigm. Younger and older adults were tested in one of three information conditions: no information control group, grandparent seminar group, and memory aging seminar group. All completed the Knowledge Memory of Aging Questionnaire (KMAQ; Cherry, Brigman, Hawley, & Reese, 2003) at pretest and posttest to evaluate changes in memory aging knowledge. All read vignettes that described forgetful younger (in their 20‘s to 30‘s) or older characters (in their 60‘s to 70‘s). Attribution ratings on the potential causes of the forgetful behavior and memory opinion ratings were solicited. All completed the Memory Functioning Questionnaire at posttest to measure selfperceived memory ability. Both age groups showed an age-based double standard in memory appraisal. Attribution and memory opinion ratings did not vary across the information groups. Only the memory aging seminar participants showed significant pre- to posttest gains on the KMAQ. Self-perceived memory functioning was significantly correlated with perceptions of forgetful characters. These data indicate that although memory knowledge improved following instruction, perceptions of forgetfulness in older adults were not influenced by increased knowledge of normative age-associated memory changes.

*

Corresponding author: Department of Psychology, Louisiana State University, Baton Rouge, LA, 70803-5501, (225) 578-8745, fax: (225) 578-4125, email: [email protected].

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Chapter 144

MEMORY RECONSOLIDATION: HISTORY, RESEARCH, AND IMPLICATIONS FOR TREATMENT OF PSYCHIATRIC DISORDERS Robert W. Flint, Jr., Karina H. Bengsz and Aeron E. Zamecnik The College of Saint Rose, Albany, NY, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Since the 1960s, research has indicated that the acquisition of new information is followed by a time-limited period of memory consolidation. During this consolidation period, the new memory exists in a labile state, where enhancing or impairing treatments are capable of modulating the subsequent strength of the memory. Considerable evidence supports the existence of a period of memory consolidation; however, following the completion of the consolidation period many scientists believed that the new long-term memory became immune to memory enhancing or impairing treatments. Over the decades, isolated studies challenged this view and suggested that old memories may sometimes become malleable again under the right circumstances. During the last 10 years a substantial body of research has developed indicating that old, previously consolidated memories may enter a state of reconsolidation when retrieved from long-term memory. In other words, the retrieval of old memories may return them to a state where they are once again susceptible to memory modulation. This chapter will review the historical development of memory reconsolidation, summarize some of the tasks, species, and treatments used in research on reconsolidation, discuss some of the important behavioral characteristics and potential mechanisms of memory reconsolidation, and consider the possible implications of this research for treatment of psychiatric conditions such as post-traumatic stress disorder, phobias, and drug addiction.

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Chapter 145

INTELLECTUAL DISABILITY: BEYOND IQ SCORES Nahal Goharpey2, David P. Crewther2 and Sheila G. Crewther1* 1

School of Psychological Science, La Trobe University, Victoria, Australia 2 Brain Sciences Institute, Swinburne University of Technology, Hawthorn, Australia

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RESEARCH SUMMARY Currently Intellectual Disability (ID) is classified as a Wechsler Intelligence Scale for Children - Fourth Edition (WISC-IV) Intelligence Quotient (IQ) below 70 and an impairment in adaptive skills during the developmental period. We suggest that the the non-verbal visual matching Raven‘s Coloured Porgressive Matrices (RCPM) should replace the commonly used WISC-IV measure of intelligence, as a means of matching groups of ID to a Typically Developing (TD) group according to their mental age, as it is a better measure of reasoning ability in children with ID who invariably have verbally based deficits. In addition, we present evidence that RCPM mental aged matched children with Low Functioning (LF) Autism, Down Syndrome (DS) and Idiopathic ID use different problem solving strategies than TD children, to achieve the same overall performance on the RCPM. This is presumably due to group differences in brain impairments as evidenced by brain imaging studies. We also present evidence from the literature that working memory is a major component of successful performance on an IQ test and that impairment in working memory in ID could affect problem solving abilities on the RCPM. The theoretical and educational implications of the discrepancy between similar overall performance level on an intelligence test, but different use of problem solving strategies are also explored.

*

Corresponding author: 400 Burwood Rd., Bundoora, Victoria, Australia 3086, [email protected], t +613 9214 5877, f +6139214 5525.

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Chapter 146

FACILITATORY EFFECTS OF MUSIC ON MEMORY: A REVIEW OF THE POTENTIAL ROLE OF EMOTIONAL AROUSAL Sherilene M. Carr and Nikki S. Rickard School of Psychology, Psychiatry & Psychological Medicine, Monash University, Australia

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Research reveals background music played during learning can variously enhance or impair memory, although the conditions which determine its effect are not yet understood. Possible explanations for the differing effects of music on memory include characteristics of the music itself, such as tempo and lyrics, induced mood of the listener and personality differences. In this chapter, consideration of the type of music used to manipulate learning and memory will be reviewed, indicating that arousal may play an important moderating role, either as a means of reducing anxiety or increasing arousal to an optimum performance levels. As music is often reported to increase arousal via emotion induction or enjoyment, a well established theory of arousal-modulated memory will be argued to underly the facilitatory effects of music on memory. The methodology used within this research paradigm will be described, and adaptations will be proposed that make it amenable to investigating the effect of music induced arousal on memory. This approach provides a novel method for combining the knowledge gained from music and memory research with arousal and memory literature to further investigate the potential memory enhancing role of music.

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Chapter 147

SPATIAL MEMORY AND LARGE-SCALE ECOLOGICAL ENVIRONMENTS Tina Iachini, Gennaro Ruggiero and Francesco Ruotolo* Department of Psychology, Second University of Naples, Caserta, Italy

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Spatial memory is a necessary prerequisite of most everyday activities. We usually define ―spatial‖ that information useful to locate objects and to interact with them. Therefore, it is ―spatial‖ information about relational and metric properties, such as relative positions (e.g., left/right), distance, size, orientation, as well as dynamic properties, such as velocity and strength. Clearly, the ability to navigate in the environment requires an understanding of all these properties and a representation in memory of structured information. To organize spatial memory, egocentric (i.e. based on body‘s position) or allocentric (i.e. based on external positions) frames of reference are used. Although research on spatial memory has a long history, in the majority of the cases experimental settings and procedures are restricted to laboratory situations, and the results are typically generalized to real world contexts. Consequently, little is known on the characteristics of spatial memory based on bodily interactions with large-scale everyday environments. In this paper we review evidence about laboratory-based and environment-based research on spatial memory. Further, a research is presented that investigated whether familiarity with a large-scale regular environment affects the spatial frames of reference necessary to represent it in memory. It was tested the hypothesis that familiarity facilitates an allocentric representation of the environment. Familiar and unfamiliar participants had to study 5 triads of buildings by walking along a path surrounding each triad. Afterwards, they had to provide relative distance judgments in relation either to their body (egocentric) or external buildings (allocentric). Results showed that familiar participants were more accurate than unfamiliar participants in the allocentric judgments and faster on the whole.

*

Corresponding author: Tel: +39-0823-274789 Fax: +39-0823-323000 E-mail: [email protected].

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356

Tina Iachini, Gennaro Ruggiero and Francesco Ruotolo

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Unfamiliar participants performed similarly in both judgments and were better than familiar participants in the egocentric judgments. These findings suggest that when the environment is familiar and regular it is represented on the basis of allocentric frames of reference. The results are discussed in relation to models of spatial memory that emphasize the importance of experience and of the geometric structure.

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Chapter 148

DOES DISREGARD OF TRANSIENT CHANGES IN THE ENVIRONMENT DIFFERENTIATE BEHAVIOUR OF CHILDREN WITH AUTISM FROM TYPICALLY DEVELOPING CHILDREN AND THOSE WITH DOWN SYNDROME AND IDIOPATHIC INTELLECTUAL DISABILITY? Nahal Goharpey, Robin Laycock1, David P. Crewther and Sheila G. Crewther 1

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

2

School of Psychological Science, La Trobe University, Victoria, Australia Brain Sciences Institute, Swinburne University of Technology, Hawthorn, Australia

RESEARCH SUMMARY In the research literature, Intellectual Disability (ID) is conceptualised as a set of unique cognitive deficits associated with particular genetic causes rather than simply low IQ. We add to this literature by exploring social/communication features that differentiate ID of three different etiologies: Low Functioning (LF) Autism, Down Syndrome (DS) and Idiopathic ID. A body of research suggests that slow shifting and/or disengaging visual attention in Autism is likely to be a major contributing factor to their impaired social and cognitive development. We propose that slow visual orienting ability in Autism is due to impairment in magnocellular processing of the visual system. Thus, we suggest that individuals with Autism are delayed in shifting and/or disengaging attention as evidenced by a disregard for transient stimuli in their environment, where as individuals with DS and Idiopathic ID show the opposite pattern, in that they appear to be unable to maintain attention to a task, being easily distracted by transient stimuli in their environment. 

Corresponding author: E-mail: [email protected]; Tel: +613 9214 5877; Fax: +613 9214 5525.

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Nahal Goharpey, Robin Laycock, David P. Crewther et al.

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The implications of this visual orienting deficit are discussed in terms of conceptualisation of Autism, visual orienting research in Autism and evidence based educational practice for children with Autism, DS and Idiopathic ID.

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Chapter 149

STUDYING MEMORY: FROM THE FRONTAL TO THE TEMPORAL LOBE AND VICE-VERSA Orlando Francisco Amodeo Bueno* Department of Psychobiology of Universidade Federal de São Paulo/UNIFESP, São Paulo, Brazil Rua Napoleão de Barros, São Paulo, SP, Brazil

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RESEARCH SUMMARY Lesions of hippocampal formation structures produce a severe global amnesia, encompassing verbal as well as non-verbal material. Since the first studies with medial temporal lobe amnesic patients, it was noted that they do not exhibit deficits of short-term memory despite the severe long-term memory impairment and this was taken as a strong evidence in favor of a subdivision of memory, that between long-term and short-term memory. The continuing studies with H.M. and other amnesic patients have led to an important discovery that gave rise to the notion of multiple memory systems. The crucial finding was that, in spite of their profound amnesia, amnesic patients usually are able to learn and retain a number of tasks. This has led to the important subdivision of memory between explicit (or declarative) episodic memory and implicit (or non-declarative memory. Implicit memory refers to retrieval independent of consciously processes. Explicit memory can be defined as the ability to store and consciously retrieve facts and events. Other fundamental finding was that the prefrontal cortex is involved with short-term memory, a concept that developed to a larger scope framework, that of working memory. The prefrontal cortex plays a crucial role in working memory, and, in particular, contributes to the functioning of the working memory episodic buffer in which multimodal information is maintained for a short time allowing for the binding of information to create integrated episodes. It has been traditionally accepted that the hippocampal system is not necessary for working memory, but, recently, this widely accepted neuroanatomic dissociation has been challenged by a number of studies that have disclosed a relationship between long-term memory and working *

Corresponding author: Telephone number: + 55 11 2149 0155, E-mail: [email protected]

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Orlando Francisco Amodeo Buen

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memory. Working memory has been shown to contribute to episodic memory formation, and the reverse also seems to occur, that is, long-term memory contributing to working memory as well. The relativelly small deficit of episodic memory in the healthy elderly can be explained by a decline in the working memory capacity and executive functions that is observed in this age. Episodic memory impairment caused by haloperidol, an antagonist of D2 dopamine receptors widely used as an antipsychotic drug, can be fully explained by the drug‘s action in the working memory capacity but not in the central executive. Other line of evidence can be found in the increasing number of work employing neuroimaging and electrophysiological recording that reveals a relationship between the prefrontal cortex activity and the temporal lobe memory system. These studies lend support to the notion of large scale connection pathways between frontal and posterior brain regions underlying and linking the functioning of the multiple memory subsystems instead of independent modules for each type of memory.

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Chapter 150

LEARNING DEFICITS IN PRESENILIN MUTANT MICE R. Lalonde1,* and C. Strazielle2 1

CHUM/St-Luc, Neuroscience Research Unit, University of Montreal, Faculty of Medicine, Montreal, Canada and University of Rouen, Faculty of Sciences, Rouen, France 2 University of Nancy, INSERM U954, Faculty of Medicine, Vandoeuvre-les-Nancy, France

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RESEARCH SUMMARY When inserted into mouse brain by transgenic or knockin methods, PS1 mutations responsible for hereditary Alzheimer's disease, despite the absence of A plaques, cause anomalies in calcium homeostasis, potentiate excitotoxicity, and alter the electrophysiologic properties of neurons. Transgenic and knockin mice with presenilin mutations are slower than age-matched controls in acquisition of spatial learning in the Morris water maze, as well as non-spatial learning in object recognition and Pavlovian trace conditioning. These detrimental effects are likely mediated either by increased A42 concentrations or by the direct action of mutated PS1.

*

Corresponding author: Email: [email protected]; Tel.: +1 (514) 890-8000; ext 35739; Fax: +1 (514) 412-7314.

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Chapter 151

ASSESSING ALERTNESS IN CHILDREN WITH PROFOUND INTELLECTUAL AND MULTIPLE DISABILITIES Carla Vlaskamp and Vera Munde University of Groningen, Department of Special Education, the Netherlands

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RESEARCH SUMMARY Assessment of cognitive, motor, sensory, and communicative functions in children with profound intellectual and multiple disabilities (PIMD) is still in its infancy. There is a lack of standardized instruments, with the instruments mainly used being checklists and observation scales. Although these lists often fail to meet the requirements of validity and reliability, they nevertheless often prove a helpful tool to determine how the person involved can best be supported. One very specific factor entailed in assessment that is related to the complexity and severity of their disabilities is the level of alertness in a child with PIMD. The assessors are often not sure when the ―best moment‖ to start an assessment is. In addition, they are often unaware of which conditions can help provoke and maintain optimal alertness levels for assessment. Alertness, however, is not just a way to optimize the assessment process; it can also be the objective of the assessment process itself. An observation list has been developed to assess the level of alertness in children with PIMD in order to 1. establish the optimal period or periods during the day to offer a stimulus or an activity; and 2. to establish the pattern of alertness in a child and the contextual influences on this pattern. In the chapter, the meaning of the concept ‗alertness‘ will be discussed. Furthermore, a description of the content of the list and its use will be presented. For this list, inter-observer and intra-observer reliability were determined by comparing the scores of three (groups of) observers: teachers, an external observer who had received additional information about the clients, and an external observer who did not know the clients at all. The results of the reliability scores for 78 situations will be presented.

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Carla Vlaskamp and Vera Munde

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The observation list seems to be a functional and sensitive instrument that provides direct support staff with the opportunity to discern individual differences in alert moments and the impact that different stimuli have on alertness. This information can be useful in clinical practice.

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Chapter 152

ASSESSMENT OF TIME PROCESSING ABILITY AND DAILY TIME MANAGEMENT IN CHILDREN WITH AND WITHOUT DEVELOPMENTAL DISABILITIES Gunnel Janeslätt1,3, Mats Granlund1,4 and Anders Kottorp2 1

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School of Health, Care and Social Welfare, Mälardalen University, Västerås, Sweden 2 Department NVS, Division of Occupational Therapy, Karolinska Institutet, Huddinge, Sweden 3 Centre for Clinical Research Dalarna, Falun, Sweden 4 School of Health sciences, Jönköping University, Jönköping, Sweden

RESEARCH SUMMARY In the time-dependent society of today, those with limited ability to manage time will show a heightened dependence on others and more need for support, exacerbating their vulnerability. Children with developmental disorders e.g. intellectual disabilities or Autism Spectrum Disorders are reported to have problems in time perception, time orientation or time management, in this chapter all related to the suggested overarching concept: time processing ability (TPA). The aim of this short communication is to present a currently developed innovative assessment of TPA and its relation to daily time management (TM) in children with and without developmental disabilities, including intellectual disabilities. The new assessment of TPA; Kit for assessing Time processing ability (KaTid) for children was based on current knowledge of information processing in children with cognitive disabilities e.g. using iconic symbols and concrete concepts. Using modern test statistics (Rasch analysis), the evaluation of the KaTid and a related Parent scale for estimating the daily TM presented acceptable psychometric properties. The results indicate that the items in KaTid, initially defined as time perception, time orientation and time management, all empirically support a potential uni-dimensional construct, TPA. In this TPA construct, time perception, time orientation and time management can be seen as different levels of complexity rather than as separate constructs. The Parent scale of daily TM also demonstrated acceptable psychometric

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Gunnel Janeslätt, Mats Granlund and Anders Kottorp

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properties. There is a relation between the parents‘ ratings of a child‘s daily TM and TPA in children with developmental disabilities. Thus TPA seems to be a factor related to children‘s daily TM that needs to be taken into consideration when planning and evaluating interventions designed to facilitate everyday functioning for children with ID. This is a step towards providing evidence-based instruments that, together with other information, can help the professional in structuring the intervention planning process for children with difficulties in daily TM.

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Chapter 153

A GEOGRAPHY OF INTELLECTUAL DISABILITIES Andrew Power Centre for Disability Law and Policy, National University of Ireland, Galway, Ireland

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RESEARCH SUMMARY People with intellectual disabilities have had a long history of exclusion and enforced dependency. As this commentary examines, the uncertainty regarding their definition and an acknowledgement that a person with an intellectual disability can be particularly vulnerable to dependency, has led to a very hidden geography for this group. From the middle of the last century, geographers examined the locational separation of people committed to the ‗idiot‘ asylums of Victorian Britain and Canada. It was clear that the asylum had a symbolic influence in the community well beyond its rather narrow role as the place of residence. More recently geographers have traced the movement of people with intellectual disabilities to group homes, co-operative housing, residence with parents and independent housing. It was hoped that the relocation from isolated stand-alone institutions would help to get rid of, or diminish stigmatisation. However, Hall1 urges us to move away from assuming that marginalisation equates solely with exclusion from mainstream social activities and spaces, and constructing inclusion as a process of incorporation into these activities and spaces. This commentary therefore forces us to take a critical approach on today‘s geography of care, where we move beyond narrow binaries of institutionalisation/ deinstitutionalisation, isolation/integration and success/failure. We must be critical of the spaces of incorporation and not assume a place of incorporation is the best choice for a person with an intellectual disability. This is particularly the case if people with intellectual disabilities face a mix of patronisation, fear, an unwillingness to understand ‗non-standard‘ forms of communication, and a strong sense of difference in public life.

1

Hall, E. (1995) The entangled geographies of social exclusion/inclusion for people with learning disabilities. Health & Place 11(1): 107-115.

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Chapter 154

PREFRONTAL MORPHOLOGY, NEUROBIOLOGY AND CLINICAL MANIFESTATIONS OF SCHIZOPHRENIA Tomáš Kašpárek* Department of Psychiatry, Masaryk University and Faculty Hospital Brno, Brno, Czech Republic

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RESEARCH SUMMARY Dysfunction of the prefrontal cortex is a hallmark of schizophrenia. This dysfunction can be demonstrated using many approaches, including functional neuroimaging techniques, neuropsychological tests focused on working and verbal memory, problem solving, or verbal fluency. Histopathological studies demonstrate the presence of cortical thickness reduction (layers II and III in particular) that is due to the neuropil loss with reduction of pyramidal neuronal size. These neuropathological changes are reflected in neuroimaging studies (volumetric studies and voxel-based studies) with findings of cortical gray matter shrinkage. All of these changes can be viewed in the context of the prefrontal disconnection that is behind many signs and symptoms of the disease, including dopamine system dysregulation and cognitive abnormalities. We review the present-day evidence for the reduction of the prefrontal cortex and then focus on the links between this abnormality and the functional and clinical features of schizophrenia.

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Chapter 155

PREFRONTAL CHOLINERGIC RECEPTORS: THEIR ROLE IN THE PATHOLOGY OF SCHIZOPHRENIA M. Udawela, E. Scarr and B. Dean Rebecca L Cooper Research Laboratories, Mental Health Research Institute of Victoria, Parkville, VIC, Australia

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RESEARCH SUMMARY There is a growing body of evidence to suggest that alterations in the cholinergic systems of the central nervous system are important in the pathology of schizophrenia. This data has arisen from studies into preclinical and clinical pharmacology, patient treatment, post-mortem neurochemistry and neuroimaging of patients with the disorder. The neuropharmacology of antipsychotics used to treat the disorder first led scientists to investigate changes in both the neurotransmitters and their receptors that are targeted by these therapeutic agents. These investigations have revealed that some atypical antipsychotics increase acetylcholine release in the prefrontal cortex, possibly contributing to improvements seen in some of the cognitive dysfunction for these drugs. Whilst there are data that show that some current atypical antipsychotic drugs have some impact on negative symptoms and cognitive deficits, none of these drugs are truly effective in treating these symptoms. Thus, in schizophrenia, various components within the cholinergic system are being investigated as potential targets for drugs that might effectively reverse these symptoms that are currently treatment-resistant. In this regard, post-mortem studies have revealed that patients with schizophrenia have low levels of cholinergic muscarinic receptors (CHRMs) in the CNS, and it is now well established that CHRM1 is decreased in the dorsolateral prefrontal cortex from subjects with the disorder; this receptor deficit is believed to play an important role in the cognitive dysfunctions associated with the disease. Recent information from basic research, in particular from studies using CHRM-/- mice, has enabled us to develop hypotheses as to what the functional consequences of deficits in CHRMs might be. Several lines of evidence also suggest a pathophysiological function for nicotinic acetylcholine receptors in schizophrenia. Nicotine administration has

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M. Udawela, E. Scarr and B. Dean

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been shown to improve cognition in patients with schizophrenia. In the prefrontal cortex this receptor is thought to affect cognition through its activation-dependent effects on dopamine D1 receptor mediated neurotransmission. Thus, both muscarinic and nicotinic receptors are viable drug targets with respect to cognitive deficits in schizophrenia. Using previous findings, in combination with our own data, we are now beginning to understand the specific changes in the various neurotransmitter receptors in the brains of schizophrenic patients, the functional effects of these changes and the roles the receptors may play in the pathology of the disorder.

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Chapter 156

THE INTERRELATIONSHIP BETWEEN DOPAMINE AND NORADRENALINE IN THE PREFRONTAL CORTEX: FROM PHYSIOLOGY TO THERAPY Ezio Carboni and Anna Rosa Carta Department of Toxicology, University of Cagliari and ―Istituto Nazionale di Neuroscience‖, Via Ospedale, Cagliari, Italy

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RESEARCH SUMMARY Dopamine release and noradrenaline release in the prefrontal cortex are required for the control of neurobiological functions, whose alteration is considered to be critical in the aetiology of widespread diseases such as schizophrenia, depression and attention deficit hyperactivity disorder (ADHD). The therapeutic agents used in treating these diseases may either increase or reduce dopamine and noradrenaline transmission by acting at receptor or at reuptake site level. The capacity of noradrenaline terminals to capture dopamine by means of the noradrenaline transporter (NET) has opened up new perspectives on the mechanism of action of norepinephine reuptake blockers such as long-established antidepressants or the new therapeutic agent for ADHD, atomoxetine. On the other hand, the hypothesis that dopamine and noradrenaline may be co-released from noradrenaline terminals in the prefrontal cortex suggests an additional interpretation of experimental evidence on the regulation of both dopamine and noradrenaline release through the pre-synaptic 2 receptor. Moreover, the high affinity of noradrenaline for the dopamine D4 receptor and its role in the prefrontal cortex, as well as the capacity of atypical antipsychotics to increase both noradrenaline and dopamine release in this area of the brain, support the hypothesis that dopamine-noradrenaline interaction may have a crucial role in the aetiology and in the therapy of schizophrenia. This chapter will illustrate and discuss the evidence for and against the hypothesis that there is an interdependence between dopamine and noradrenaline transmission in the prefrontal cortex, taking into consideration some recent evidence from our laboratory on the effect of chronic treatment with methylphenidate and atomoxetine on dopamine and noradrenaline release in the prefrontal cortex.

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Chapter 157

PARTICIPATION OF THE PREFRONTAL CORTEX IN THE PROCESSING OF SEXUAL AND MATERNAL INCENTIVES Marisela Hernández González and Miguel Angel Guevara Instituto de Neurociencias, Universidad de Guadalajara, Jalisco, México

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RESEARCH SUMMARY Sexual and maternal behaviors constitute motivated behaviors, the adequate manifestation of which requires an appropriate integration of external stimuli and internal states. In both is required the perception of an appropriate stimulus. For a male rat, one appropriate sexual incentive stimulus could be a receptive female, while for a female mother rat the appropriate maternal incentive could be a pup rat. The sensory clues emitted by either the potential sexual partner or the pups must be first detected and then processed in order to be perceived as incentives and as potentially rewarding. The prefrontal cortex (PFC) plays an important role both in mediating the assignation of the incentive value and in information processing. Thus, using electroencephalographic (EEG) recordings, we have characterized the prefrontal functioning during motivational states of sexual and maternal behavior in rats. In a first study, it was observed that the EEG activity of the medial (mPFC) and orbital prefrontal cortices (oPFC) was modified during the performance of male rats in a T-maze under two different conditions: sexually-motivated (with previous intromission and one receptive and one non-receptive female placed in the goal boxes of the lateral arms); and not sexuallymotivated (no previous intromission and empty goal boxes). Only the sexually-motivated males showed a higher proportion in the 6-7 Hz band and a lower proportion in the 8-11 Hz band during the awake-quiet state and while walking in the maze stem. In addition, they showed an increased correlation of the 6-7 Hz band while walking in the maze stem and when remaining close to a receptive female. Similar EEG changes were obtained in estrous female rats that were subjected to a sexually-motivated task using the same paradigm of the T-maze. In the oPFC of the sexually-motivated females and males, different EEG patterns were 

Tel: (52) 33 38 18 07 40 ext 5860; E-mails: [email protected]; [email protected].

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Marisela Hernández González and Miguel Angel Guevara

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observed, results that suggest a different functionality of the mPFC and oPFC, which may work together in the processing of sexual incentive stimuli. Another study explored whether the mPFC of female rats shows characteristic EEG patterns during the presentation of olfactory stimuli, when (1) associated with pups (nest-bedding); and, (2) not-associated, with pups (female bedding), during the following distinct reproductive states: proestrus-estrus (PE), diestrus (D) and lactation (L). During the smelling of nest-bedding, only the L rats showed a higher proportion in the 8-11 Hz band. This finding may represent a characteristic processing of the olfactory stimuli related to pups in the mPFC of L rats. Taken together, these data allow suggest that in rats the prefrontal cortex participates in identifying and processing sexual and maternal incentives.

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Chapter 158

FROM CONFLICT TO PROBLEM SOLUTION: THE ROLE OF THE MEDIAL PREFRONTAL CORTEXIN THE LEARNING OF MEMORY-GUIDEDAND CONTEXTADEQUATE BEHAVIORAL STRATEGIES FOR PROBLEM-SOLVING IN GERBILS Holger Stark Leibniz Institute for Neurobiology, Magdeburg, Germany

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RESEARCH SUMMARY We conducted an investigation of the way in which animals acquire problem-solving behavioral strategies. The focus was on the search for sequential feedback rules that guide an individual along the stepwise learning process from the initial conflict generated by a novel situation to the context-adequate, problem-solving and, therewith, successful behavioral strategy. The medial prefrontal cortex plays a complex role in acquisition and storage of behavioral strategies. It is an important part of the internal reward system, inducing a motivational drive for the development of a memory-guided, goal-directed behavioral strategy. This view is also strongly supported by our work on the learning-related dynamics of prefrontal dopamine release. Using Mongolian gerbils (Meriones unguiculatus) as an animal model, we found that the formation of an avoidance strategy in a shuttle-box during the stage of avoidance learning is accompanied by a strong increase of the activity in the prefrontal dopamine system. Cortical theta activation was found to be, overall, negatively correlated with the formation of avoidance strategy during learning. In learning stages preceding the stage of avoidance learning we found different decreases of theta activity. However, when the animals entered the stage of avoidance learning, i.e., the phase when prefrontal dopamine release increases, theta activity increased again as well. A detailed analysis of theta activation revealed unique

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Holger Stark

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events in single trials marking the transition between behaviorally-defined learning stages and reflecting the actual change of the task-context for the animal. Based on the correlation between behavioral data and data of learning-relevant physiological parameters, i.e., prefrontal dopamine and theta activation, we discuss cognitive processes like feedback learning, error processing, planning, decision making, and short-term memory as components of working memory functions during stepwise learning. The detailed analysis of learning processes in simple avoidance conditioning paradigms is a prerequisite for a deeper understanding of information processing during the goal-directed formation of behavioral strategies.

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Chapter 159

THE ORBITOFRONTAL CORTEX AND EMOTIONAL DECISION-MAKING: THE NEGLECTED ROLE OF ANXIETY Sabine Windmann and Martina Kirsch Goethe University, Department of General Psychology II Institute of Psychology and Sports Sciences, Frankfurt/Main, Germany

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RESEARCH SUMMARY The orbital part of the prefrontal cortex is known to be crucially involved in emotional decision-making. Its function seems to be, first, to associate affective value with behavioral bias (i.e., approach or withdrawal) in complex choice situations, and secondly, to flexibly control and transiently inhibit affective and behavioral impulses. Dysfunction of this region due to damage or immaturity of OFC cells leads to impulsiveness, behavioral perseveration, and reduced sensitivity for risk, as observed in children as well as various patients groups. We review the evidence with a focus on the much less investigated question of whether and how hyperactivation (or hyperfunctioning of modules and processes) involving OFC leads to the opposite behavioral tendencies, namely risk-aversion, enhanced inhibition, undecidedness and higher risk sensitivity including heightened anxiety. We identify two perspectives with opposing views onto this issue, and report some unpublished studies of populations with children and patients with anxiety disorders using the Iowa gambling task, a task that is presumed to be sensitive to OFC function. We find that, if anything, anxiety has the same beneficial effects onto performance as cortical maturation. Although effects of anxiety are much weaker and less conclusive than those of age during childhood, it seems that there are situations in which enhanced anxiety can support advantageous decision-making.



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Sabine Windmann and Martina Kirsch

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Our results highlight the important role of orbitofrontal cortex in integrating approachand withdrawal-tendencies mediated by mesolimbic and mesostriatal structures on the one hand and higher cognitive centres on the other, with the latter ones recruiting more dorsal parts of the prefrontal cortex and allowing for conscious thinking, reasoning, and problemsolving. Behavioral interventions as in education, cognitive training, and psychotherapy are most effective when they take into account the motivational and evaluative function of this region.

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Chapter 160

PEEF: PREMOTOR EAR-EYE FIELD. A NEW VISTA OF AREA 8B Bon Leopoldo, Marco Lanzilotto and Cristina Lucchetti Department of Biomedical Sciences, University of Modena and Reggio Emilia, Modena, Italy

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RESEARCH SUMMARY In macaque monkeys, area 8B may be considered cytoarchitectonically as a transitional area between the granular area 9, rostrally, and the rostral part of the dorsal agranular area 6 (FC or F7), caudally. This area is anatomically connected with auditory cortical areas, cerebellum and superior colliculus. Microstimulation of area 8B evokes ear movements or eye movements in some sites; in other sites, it evokes both ear and eye movements by varying the intensity of electric stimulation. Unit activity recording shows that neurons in area 8B have a role in encoding different auditory environmental stimuli and movements of the ear and eye. In addition, fixation of a visual stimulus, when attention is engaged, modulates the discharge of auditory environmental neurons, and sensory-motor neurons. Current functional and anatomical evidences strongly support the proposal that area 8B is a specific Premotor Ear-Eye Field (PEEF) involved in the recognition of auditory stimuli and in orienting processes. Moreover, activation by specific environmental auditory stimuli, suggests that PEEF is an important node in the hierarchical organisation of the auditory network. The inhibitory effects on neural discharge of auditory and auditory-motor cells might be a consequence of the engagement of attention during visual fixation. This phenomenon may be the expression of a combination of a covert orienting of attention relative to eye effectors, and an overt orienting of attention relative to ear effectors. It seems that attention may affect more than one channel at the same time during a conditioned task or during natural behaviour. Then the PEEF, based on its connections and functional characteristics may be involved in three circuits: 1) an auditory circuit, 2) an oculomotor circuit, 3) and a fronto-cerebellar circuit.

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Chapter 161

PREFRONTAL CORTEX: ITS ROLES IN COGNITIVE IMPAIRMENT IN PARKINSON’S DISEASE REVEALED BY PET Qing Wangab, Kelly A. Newella, Peter T. H. Wongd and Ying Luc

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Neurobiology Research Centre, School of Health Sciences, University of Wollongong, Australia Department of Neurology, the Third Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, P.R.China Department of Radiology and Biostatistics, University of California, San Francisco, CA, US Departments of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

RESEARCH SUMMARY Parkinson‘s disease (PD) is a neurodegenerative disorder, classically characterized by the chronic loss of dopaminergic neurons primarily in substantia nigra pars compacta, which leads to a reduction of dopamine levels in the striatum. The motor symptoms do not become obvious until at least an 80% reduction in striatal dopamine levels. Recent works have demonstrated that cognitive impairment occurs even in the early course of PD which is correlated with dopaminergic dysfunctions in the prefrontal cortex and not necessarily related to motor disorders. This commentary will discuss the current knowledge of the prefrontal cortex and its association with cognitive deficits in PD. Increasing evidence show that profound dopamine depletion not only occurs in the striatum but also in the prefrontal cortex, and this may be associated with the cognitive deficits in PD. L-dopa is widely used for the treatment of PD and shows beneficial effects on



Corresponding author: Dr. Qing Wang, Neurobiology Research Centre, School of Health Sciences, University of Wollongong, NSW 2522, Australia. Phone: +61 2 4221 3199; Fax: +61 2 4221 4096; Email: denniswq@ yahoo.com or [email protected].

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Qing Wangab, Kelly A. Newella, Peter T. H. Wongd et al.

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the cognitive dysfunctions among PD patients. One study by Shohamy, based on electrophysiological and computational examination, demonstrated that the loss of dopamine in PD led to specific learning impairment, and that enhancing dopamine levels with L-dopa treatment alleviated the impairment of feedback-based sequence learnin. Mollion also showed that in two conditional associative learning tasks, the increase in response time and the decrease in errors found in L-dopa medicated PD patients compared to non-L-dopa medicated patients reflected enhancement of working memory, suggesting the L-dopa treatment improve the cognitive impairment in PD patients. More evidence indicated that mesocortical regions, especially prefrontal cortex, may be the key locus for cognitive functional improvement following dopaminergic enhancement. Interestingly, L-dopa was also found to exert detrimental effects on cognition related functions like extinction learning and probabilistic reversal learning. For these contrasting effects, Cools proposed that increases of dopamine transmission in prefrontal cortex and its reductions in striatum contribute to the cognitive stability; however, cognitive flexibility benefited from potentiated phasic striatal dopamine transmission and its reduction in the prefrontal cortex.

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Chapter 162

NORADRENERGIC ACTIONS IN PREFRONTAL CORTEX: RELEVANCE TO AD/HD Amy F. T. Arnsten Yale Medical School, New Haven, CT, US

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RESEARCH SUMMARY This chapter reviews the important role of prefrontal cortex (PFC) in the regulation of behavior and attention, and evidence that these processes are weakened in AttentionDeficit/Hyperactivity Disorder (AD/HD). Norepinephrine (NE) has been found to have a critical beneficial effect on PFC function through actions at post-synaptic, 2Aadrenoceptors, while high levels of NE release during stress impair PFC regulation of behavior through actions at 1 adrenoceptors. The PFC regulates its own NE input through projections to NE-containing locus coeruleus (LC) neurons. The LC fires according to arousal state and attentional demands. Most medications effective for the treatment of AD/HD powerfully influence NE transmission, either by blocking reuptake or mimicking its actions at 2A-adrenoceptors. The importance of NE to AD/HD is increasingly appreciated.



Correspondence to: Dr. Amy F.T. Arnsten. Department of Neurobiology, Yale Medical School, 333 Cedar St., New Haven, CT 06510; Email: [email protected]; Phone: 203-785-4431; Fax: 203-785-5263.

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Chapter 163

PREFRONTAL CORTEX: BRODMANN AND CAJAL REVISITED Guy N. Elston1 and Laurence J. Garey2 1

Centre for Cognitive Neuroscience, Sunshine Coast, Australia 2 Centre for Psychiatric Neuroscience, Lausanne, Switzerland

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RESEARCH SUMMARY Modern imaging techniques allow the mapping of gross brain structure to an exacting standard; however, these methodologies have been applied inappropriately in recent times to the study of the prefrontal cortex – the structure identified by Brodmann as being central to intelligence. Currently, these methodologies cannot detect prefrontal cortex, nor be used to quantify it. Here we review Brodmann‘s data on comparative aspects of the gross structure of the cerebral cortex, some of which have been largely ignored in recent times. We believe this still remains the definitive data set for prefrontal cortex. In addition we compare Brodmann‘s observations with those of his contemporary Santiago Ramon y Cajal. Cajal‘s studies of the fine structure of the cerebral cortex led him to the conclusion that human intelligence is largely attributable to the complexity of the pyramidal (psychic) cell. These observations are compared and contrasted with modern data on prefrontal cortex, essentially substantiating the conclusions of these two great founding fathers of modern neuroscience.

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Chapter 164

DEVELOPMENTAL CHARACTERISTICS IN CATEGORY GENERATION REFLECTS DIFFERENTIAL PREFRONTAL CORTEX MATURATION Julio Cesar Flores Lázaro1,2 and Feggy Ostrosky-Solís1* 1

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Universidad Nacional Autónoma de México, Psychology Faculty, Laboratory of Neuropsychology and Psychophysiology México, D.F. 2 Universidad Juárez Autónoma de Tabasco, División Académica de Ciencias de la Salud, Villahermosa Tabasco, México

RESEARCH SUMMARY The developmental characteristics of semantic category generation were studied in a sample of 200 neurologically intact subjects from 6 to 30 years old. Results indicate that diverse brain areas support different the category criteria used: subjects in the 6-8 age range used a concrete criteria (posterior brain areas), in the 9-11 age range a functional criteria is dominant (dorsolateral prefrontal cortex), while abstract criteria becomes dominant in the 1214 age-range (anterior prefrontal cortex) and continuous to develop in the 16 to 30 age range. It is proposed that different prefrontal areas participate during development, shaping cognitive approach to categorisation during childhood and adolescence.

*

Correspondence: Feggy Ostrosky-Solís, Universidad Nacional Autónoma de México, facultad de Psicología, Laboratorio de Neuropsicología y Psicofisiología. Rivera de Cupia 110-71. Lomas de Reforma. México D.F. C.P. 11900. E-mail address: [email protected].

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Chapter 165

WORKING MEMORY AND THE AUTISTIC MIND R. Hansen, L. Deling, E. Olufs, R. Pytlik and F. R. Ferraro* University of North Dakota, Grand Forks, ND, US

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RESEARCH SUMMARY The current chapter will focus on working memory abilities and development, primarily examining individuals with autism ages 5 to 20 years. With Baddeley and Hitch‘s model as a starting point, we will explore the research surrounding how working memory typically develops, deviations found in the autistic population compared to typical working memory performance and development, and the role such differences may play when considering possible intervention strategies to use with individuals with autism spectrum disorders. Recent findings in the working memory literature will be examined, including task effects that facilitate and inhibit performance, experimental design factors that may play a role in the contradictory results within the area of working memory in individuals with autism spectrum disorders, and neurological factors that may contribute to cognitive differences. In general, working memory capacity increases with age in the typically developing population, with specific increases seen in short-term memory capabilities, verbal span abilities, visual span abilities, and complex working memory processes. Specialized working memory components and strategies also develop with age. There is currently little evidence of a general working memory deficit in individuals with autism; however, research suggests that certain domains of working memory may show impairments or delayed development in individuals with autism. Verbal span abilities appear to be largely intact within the ASD population with deficits on tasks that rely on spontaneous rehearsal strategies that prove helpful as the task complexity increases. The visuospatial sketchpad of children and adolescents with autism seems grossly intact with some deficits demonstrated in oculomotor

*

Corresponding author: Chester Fritz Distinguished Professor, Director, General/Experimental Ph.D. Program, Fellow, National Academy of Neuropsychology, Dept. Psychology - University of North Dakota, CorwinLarimore Rm. 215, 319 Harvard Street Stop 8380, Grand Forks, ND 58202-8380, 701-777-2414 (O), 701-7773454 (FAX), and F. R. Ferraro, [email protected].

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R. Hansen, L. Deling, E. Olufs, R. Pytlik et al.

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and spatial tasks requiring more mature development. Within the central executive, studies have shown individuals with autism to have intact performance on simple inhibition tasks. However, they often show impaired performance on measures of planning and complex inhibition tasks. On tasks that involve the episodic buffer component, children and adolescents with autism tend to encode specific features of events rather than global features, making memory strategies less efficient. Some of these deficits have been attributed to neurobiological differences found in individuals with autism, including an increased total brain volume, overreliance of the right hemisphere, reduced activation of the dorsolateral prefrontal cortex, atypical activity in the cingulate cortex, and underconnectivity in several circuitry systems. Although little research has specifically been conducted on working memory interventions for individuals with autism, understanding specific working memory strengths and weaknesses can help guide approaches to improving working memory functioning. Within other populations, working memory training has been effective in targeting specific working memory factors that are possibly implicated in autism as well, including metamemory skills, overt rehearsal strategies, and elaboration. Additional research is needed on the capacity and development of working memory in children with autism as current findings are often inconsistent.

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Chapter 166

MEASUREMENT OF WORKING MEMORY Karlee D. Fellner1 and John R. Reddon2 1

University of British Columbia, Vancouver, British Columbia, Canada 2 Alberta Hospital Edmonton, Edmonton, Alberta, Canada

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RESEARCH SUMMARY Working memory is the mechanism involved in the temporary manipulation and storage of information. It contributes to a number of cognitive functions, including learning, retrieving long-term memory, inhibiting irrelevant information, and working with novel problems. Working memory has limited capacity, and thus has significant implications for individual differences in learning and cognitive functioning. Measurement of working memory is used to assess intellectual and cognitive ability, including individual cognitive development and declines and deficits in performance related to aging, dementia, neurological disorders, medical conditions, genetic disorders, developmental disabilities, learning disabilities, and psychiatric conditions. Working memory tasks include simple span (visuospatial and phonological short-term memory) and complex span tasks (visuospatial, phonological, and executive working memory). Commonly used memory assessment scales include the Wechsler Memory Scale, Wide Range Assessment of Memory and Learning, Swanson Cognitive Processing Test, Working Memory Test Battery for Children, and Automated Working Memory Assessment. Cognitive scales which contain an assessment of working memory include the Wechsler intelligence scales, Cognitive Assessment System, Stanford Binet Intelligence Scale, Woodcock-Johnson, Differential Ability Scales, Kaufman Assessment Battery for Children, Universal Nonverbal Intelligence Test, and NEPSY Developmental Neuropsychological Assessment. Despite the number of measures designed to assess working memory, there is controversy over the consistency and overall adequacy of its measurement. This is largely because it is challenging to measure working memory directly, as it is influenced by factors such as processing speed, knowledge, executive functioning, long-term memory, and attention. In addition, tasks provide only a small sample of overall working memory.

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Karlee D. Fellner and John R. Reddon

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Also problematic is that working memory itself is a complex construct that is not fully understood by the scientific community. Controversy aside, the assessment of working memory is essential in the measurement of cognitive functioning in order to identify individual strengths and weaknesses and to inform individual remediation/treatment.

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Chapter 167

EFFECTS OF VISUO-SPATIAL WORKING MEMORY ON WAYFINDING ABILITY Laura Piccardi1,2 and Raffaella Nori3 1

2

Department of Health Sciences, University of L'Aquila, Italy Research Centre of Neuropsychology, IRCCS Foundation, Saint Lucia, Rome, Italy 3 Department of Psychology, University of Bologna, Italy

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RESEARCH SUMMARY The present review analyse the relationship between visuo-spatial working memory (VSWM) in wayfinding, which is the ability to move successfully through the environment. As the results of research on individual differences in wayfinding are mixed, various explanation have to be considered. In this chapter, we will analyze these findings in light of the different component of VSWM proposed by Logie (1995, 2003) and a more recent model by Cornoldi and Vecchi (2003). We will also investigate the development of VSWM and how its changes in older adults, causing a decrease in wayfinding ability. For example, evidence from studies of route learning and memory for object location indicates an aging-related decrement in piloting, particularly in unfamiliar surroundings. On the one hand, the decline in landmark-based navigation could be the result of diminished path integration skill, particularly if path integration typically provides a supplemental informational for piloting. On the other hand, the more basic path integration process may retain its operational integrity beyond the time that association-based piloting begins to reflect a general age-related decline in learning rate. In this chapter, we considered these different explanations in relation to theories about VSWM. Finally, we consider the results of studies on brain-damagedpatients demonstrating the importance of the ventromedial prefrontal cortex, which is necessary to maintain active the goal destination in VSWM for use in navigation.

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Chapter 168

WORKING MEMORY AND PREFRONTAL CORTEX AND THEIR RELATION WITH THE BRAIN REWARD SYSTEM AND DRUG ADDICTION Ester Miyuki Nakamura-Palacios Laboratory of Cognitive Sciences and Neuropsychopharmacology, Department of Physiological Sciences, Health Science Center, Federal University of Espírito Santo, Vitória-ES, Brazil

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RESEARCH SUMMARY Cellular and molecular mechanisms involved in learning and memory processes are very similar or the same as those involved in the drug-induced reorganization of neural circuitry that occurs during addiction. Using a classic working memory task in animal learning, the radial maze, we have demonstrated that different drugs of abuse (for instance, ethanol, 9tetrahydrocanabinol and nicotine) administered into the medial prefrontal cortex (mPFC) affect the performance of a delayed-task, suggesting that these drugs somehow change the spatial working memory processing. These effects may involve dopaminergic and/or glutamatergic mediation in the mPFC because they were prevented by SCH 23390, clozapine or memantine. The mPFC in rodents, which is functionally related to the dorsolateral prefrontal cortex (DLPFC) in primates and human beings, is part of the brain reward circuitry and highly involved in the processing of working memory. Working memory manipulates items in short-term memory to plan, organize, and process information required to generate future thoughts or actions. Its integrity is required in the processing of important cognitive functions such as learning, goal-directed behavior, decision-making, understanding and reasoning, all function that are substantially affected in drug addiction and dependence. In a randomized double-blind placebo-controlled clinical trial we showed that gabapentin, an anticonvulsant drug, reduced alcohol consumption and craving, and also improved frontal cognitive performance involving working memory processing. In a recent study considering different types of alcoholics according to Lesch‘s typology we found that frontal dysfunction was more seen to a greater extent in Type IV alcoholics, even in those that showed preserved

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Ester Miyuki Nakamura-Palacios

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mental function measured by mini-mental status examination. Considering this pitiful evidence, we started to search for any treatment that would possibly decrease this frontal cortical dysfunction, especially the processing of working memory. We found interesting data showing that transcranial direct current stimulation (tDCS) over the left DLPFC improved the working memory and reduced alcohol craving. Thus, we are currently investigating the effects of tDCS over the left DLPFC in the P3 waveform registered by Event Related Potential (ERP) in alcoholics. So far, in a sample of alcoholics, we have found that tDCS results in a change the P3 waveform in frontal and central region that may be related to changes in brain activity. Completion of this study and adding future investigations that combine pharmacological and non-pharmacological strategies may unravel this intriguing relationship between working memory in the prefrontal cortex and drug addiction, and hopefully establish new therapeutic possibilities.

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Chapter 169

WORKING MEMORY IN THE SERVICE OF VERBAL EPISODIC ENCODING: A COGNITIVE NEUROPSYCHOLOGICAL PERSPECTIVE Matthew J. Wright1, Peter Bachman2 and Ellen Woo3 1

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Psychology Division, Department of Psychiatry, Harbor-UCLA Medical Center, Torrance, CA, US 2 Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, UCLA David Geffen School of Medicine, Los Angeles, CA, US 3 Mary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, UCLA David Geffen School of Medicine, Los Angeles, CA, US

RESEARCH SUMMARY While dissociations between working memory and episodic memory have been shown, both of these processes appear to partially overlap at the behavioral and neuroanontomical levels. Episodic encoding and working memory both appear to depend on the integrity and integration of processes carried out within the lateral prefrontal cortex and both appear to be related to effective verbal learning. The neuroanatomic substrate of semantic memory also appears to overlap with these processes in the prefrontal cortex. In the current chapter, we review interactions between verbal working memory, semantic memory, and episodic memory in individuals suffering from closed head injury, human immunodeficiency virus/acquired immunodeficiency syndrome, Alzheimer‘s disease, and Schizophrenia in an attempt to elucidate the cognitive neuropsychology of verbal memory encoding. Our review suggests that working memory enhances encoding, but not retention, of verbal episodic memories across these memory-disordered populations.

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Chapter 170

WORKING MEMORY IN PRETERM AND FULL-TERM INFANTS Jing Sun* and Nicholas Buys Griffith Health Institute, Griffith University, Australia

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RESEARCH SUMMARY Introduction: This study investigated working memory in preterm and full-term infants at 8 months after expected date of delivery. Working memory is defined as ―the ability to maintain an appropriate problem solving set for the attainment of a future goal‖. An important characteristic of working memory is that it is prospective, that is, its purpose is to attain a goal, and it not only enables information to be held in mind but also to be manipulated. Working memory emerges in infancy and continues to develop throughout childhood. Working memory is believed to underlie some learning problems in children at school age. Although numerous studies have reported that the overall development of preterm infants is comparable to that of full-term infants at the same corrected age, it is unclear to what extent the development of specific cognitive abilities is affected by prematurity and/or other factors such as medical complications. As preterm infants have a high rate of learning difficulties, it is possible that factors associated with prematurity specifically affect the development of some regions of the brain associated with the regulation of working memory. Methods: The current study aimed to examine the effects of maturation and length of exposure to extrauterine environmental stimuli on the development of working memory, by comparing the development of preterm infants with that of full-term infants at both the same corrected age and the same chronological age. A case-control study design was used for the study. Thirty-seven preterm infants without identified disabilities and 74 full-term and gender matched healthy full-term infants participated in the study.

*

Corresponding author: [email protected]; School of Public Health, Griffith University, & Griffith Health Institute, Griffith University Meadowbrook Q4131 Australia.

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Jing Sun and Nicholas Buys

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The preterm infants were all less than 32 weeks gestation and less than 1500 grams birthweight. All infants were assessed on working memory tasks at 8 months after the expected date of delivery (when preterm infants were actually 10-11 months chronological age). Results: The findings of the study showed that preterm infants performed significantly more poorly than full-term infants at 8 months after the expected date of delivery on measures of working memory. The results suggest that the effects of maturation are greater than the effects of exposure to extrauterine environmental stimuli on the development of working memory. Furthermore, the preterm infants were divided into two subgroups on the basis of (a) low or high medical risk factors, (b) birthweight of < 1000 g versus 1000-1500 g, and (c) gestation age of < 28 weeks versus 28-32 weeks, in order to assess the effects of these variables on the performance of working memory. Medical risk, lower birthweight and lower gestation age were all found to adversely affect performance on working memory. Discussions and Conclusions: It is argued that medical risk, lower birthweight and lower gestation factors may influence the development of specific areas of the brain which govern working memory, and given that the prefrontal regions are particularly immature they may be especially vulnerable to damage or disruption. The present study provides further insights into the emergence of working memory in infants and the feasibility of evaluating these abilities in infants who are at risk for further learning difficulties and attention deficits.

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Chapter 171

THE ASSESSMENT AND TRAINING OF WORKING MEMORY FOR PREVENTION AND EARLY INTERVENTION IN CASE OF READING, WRITING AND ARITHMETICAL DIFFICULTIES IN CHILDREN Antonella D’Amico Department of Psychology, University of Palermo, Palermo, Italy

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RESEARCH SUMMARY The first part of the chapter reviews the recent literature regarding the involvement of working memory functions in scholastic learning and its role as an underlying factor of reading, writing and arithmetical difficulties. In the second part of the chapter we find an experience of assessment and training of working memory for the prevention of reading, writing and mathematical learning difficulties. On the basis of this study, an Italian working memory test battery and a training programme have been developed, including a series of activities involving both verbal and visual-spatial working memory with different degrees of central executive demand.

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Chapter 172

WORKING MEMORY IN SENTENCE COMPREHENSION AND PRODUCTION Matthew J. Traxler*1, David Caplan2, Debra L. Long1 and Gloria S. Waters3 1

2

University of California, Davis, CA, US Massachusetts General Hospital, Harvard University 3 Boston University, Boston, MA, US

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RESEARCH SUMMARY Sentence comprehension and production both involve temporary activation, storage, and manipulation of partially structured representations. Comprehenders sometimes buffer individual words and phrases as they register and process new input and relate new to previously presented input. Speakers must activate conceptual representations, search for corresponding lexicalized concepts, place them in the appropriate order, and apply the proper inflections before they can begin articulation. All of this activity requires some ability retain information in an active state and manipulate this information. Considerable research on both healthy and neurologically impaired individuals has focused on describing the working memory system or systems that support this temporary activation and manipulation of information. This paper provides an overview of the theoretical and methodological issues that characterize research in this area, with a particular emphasis on sentence processing. We will make a number of suggestions for improving the methods used to research working memory in sentence comprehension and production.

*

Address Correspondence to:Matt Traxler, Department of Psychology, UC Davis, 1 Shields Avenue, Davis, CA 95616, 530 752 2087 (fax) 530 902 8526 (o), [email protected].

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Chapter 173

WORKING MEMORY COMPONENTS AND VIRTUAL REORIENTATION: A DUAL-TASK STUDY Alessandro O. Caffò, Luciana Picucci, Manuela N. Di Masi and Andrea Bosco University of Bari, Bari, Italy

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RESEARCH SUMMARY In the history of cognitive psychology, one of the most studied, analyzed, cited, revised and criticized theoretical model was the Baddeley & Hitch's (1974) Working Memory Model. A binding attribute of working memory is its limited capacity, as evidenced by the studies on span measures. The methodology most often used to investigate such limited capacity is dualtask paradigm. In the present experiment a dual task procedure was employed to evaluate the requirements of working memory resources in a virtual spatial memory task. In previous studies, a dual task procedure was employed to shed light on the hypothesis that spatial language would be an essential for the integration of geometric and non-geometric (feature) information. Nowadays, contrasting results do not permit to accomplish with this hypothesis and integration of different classes of information remains at level of open debate. The present experiment was aimed at providing new evidence for the aforementioned topic employing the virtual version of the reorientation task) and two well-known concurrent tasks: articulatory suppression for verbal and spatial tapping tasks for visuo-spatial working memory components, respectively. These tasks were already employed in navigation-based experiments. If visuo-spatial working memory is substantially involved in reorientation, then it might expect that spatial tapping would impair the encoding relationships among target, landmark and geometric characteristics of the environment largely than articulatory suppression. On the other hand, a large decrease in performance following articulatory suppression will lead to conclude that the language hypothesis might be correct. Sixty participants were randomly assigned to one of three different dual task experimental conditions:

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Alessandro O. Caffò, Luciana Picucci, Manuela N. Di Masi et al.

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Articulatory Suppression Task, Spatial Tapping Task and No Concurrent Task. The articulatory suppression task involved a sequence of monosyllabic syllables when pronounced by Italian speakers i. e. Ba/Be/Bi/Bo/Bu/Da/De/Di/Do/Du. The spatial tapping task involved the participant in tapping repeatedly on wooden keys of a custom-made keypad. Data showed a main effect of the dual task interference, with a significant decrease in performance as effect of visuo-spatial as well as verbal dual task. Moreover, the difference between the two dual tasks was also significant demonstrating that visuo-spatial interference worsened the performance significantly more than verbal one. These results seem to shed new light on current debate, since they lead to conclude that reorientation task engages critically visuo-spatial, and with a minor extent, verbal component of working memory.

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Chapter 174

USING FMRI TO EXAMINE THE BRAIN: BASES OF WORKING MEMORY Michael A. Motes1,2,*, Ehsan Shokri Kojori1, Neena K. Rao1, Ilana J. Bennett1 and Bart Rypma1,2 1

Center for BrainHealth & School of Behavioral and Brain Sciences, University of Texas at Dallas, TX, US 2 Department of Psychiatry, University of Texas Southwestern Medical Center, TX, US

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RESEARCH SUMMARY Considerable knowledge has been gained about the brain bases of working memory through research with functional magnetic resonance imaging (fMRI). However, using fMRI to explore the component processes that support working memory is difficult due to the timing of component processes and the lag of the hemodynamic response underlying the blood oxygen level dependent (BOLD) response in fMRI. Resolving controversies regarding the role of various brain regions in encoding, maintaining, retrieving, searching, and comparing information held in working memory requires isolating BOLD signal changes in response to the engagement of each of these component processes. A variety of fMRI experimental design and analysis techniques have been used for this purpose. These have included regression analyses with models based on canonical or subject-derived hemodynamic response functions, varying the duration of component process intervals, using component process intervals that exceed the ideal time needed for the hemodynamic response to return to baseline, regression modeling of parts of component process intervals, and including partial-trials in which only a subset of the component processes are engaged.

*

Corresponding author: Center for BrainHealth, University of Texas at Dallas, 2200 W. Mockingbird Lane, Dallas, TX 75235, Phone: 972-883-3254. Fax: 972-883-3231, Email: [email protected].

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Michael A. Motes, Ehsan Shokri Kojori, Neena K. Rao et al.

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The present chapter provides an overview of the technical challenges in using fMRI to examine the brain bases of working memory component processes, briefly reviews study designs and analysis methods that have been used to explore the brain bases of working memory, and offers suggestions for future research directions.

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Chapter 175

AGING AND SHORT-TERM MEMORY FOR FACE IDENTITY OF EMOTIONAL FACES Sandra J. E. Langeslag* and Jan W. van Strien Erasmus Affective Neuroscience Lab, Institute of Psychology, Erasmus University Rotterdam, The Netherlands

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RESEARCH SUMMARY Age differences have been observed in emotional modulation of long-term memory (LTM) but have not yet been investigated in short-term memory (STM) in a comparable manner. In this study, age differences in the effect of stimulus emotionality on STM for stimulus content were examined. Younger (18-29 years) and older (61-77 years) adults completed a STM task with angry, happy, and neutral faces. Memory for face identity was increased for angry and neutral compared to happy faces. The response bias was most conservative for angry, and most liberal for happy faces. No age differences were observed in this emotional modulation of STM. It is argued that this is not due to lack of statistical power or to participant characteristics, but rather to the constraint nature of the task (probe-guided retrieval and short retention interval). The current findings do not suggest that emotional modulation of STM changes across the lifespan.

*

Corresponding author S. Langeslag is now at: Erasmus MC – Sophia Children‘s Hospital, Department of Child and Adolescent Psychiatry, P.O. Box 2060, NL-3000 CB Rotterdam, The Netherlands, Email address: [email protected]. Tel: +31 (0)10 703 7071. Fax: +31 (0)10 703 2111.

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Chapter 176

VARYING BACKGROUND COLOURS REVEALS THAT ENHANCED SHORT-TERM MEMORY FOR ANGRY FACES IS A VALENCE AND NOT AN AROUSAL EFFECT Sandra J. E. Langeslag1*, Margaret C. Jackson2, Jan W. van Strien1 and David E. J. Linden2 1

Erasmus Affective Neuroscience Lab, Institute of Psychology, Erasmus University Rotterdam, The Netherlands 2 Wolfson Centre for Clinical and Cognitive Neurosciences, School of Psychology, Bangor University, UK

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY There is debate on whether the effect of stimulus emotionality on memory is a valence or an arousal effect. In a previous study, short-term memory (STM) was enhanced for angry compared to happy and neutral faces, and music-induced contextual arousal did not modulate this effect. The absence of such a contextual arousal effect could, however, have been due to the cross-modal nature of the study, as the contextual arousal was induced auditorily while the to-be-remembered stimuli were presented visually. In this study, we investigated the influence of visually-induced contextual arousal on the same STM task to determine whether the angry face benefit in STM is a valence or an arousal effect. Contextual arousal was successfully manipulated by presenting the background colours red, pink, and light pink. STM discrimination was enhanced for angry faces, and was not modulated by contextual arousal. High contextual arousal elicited by the red or pink backgrounds was accompanied by a more liberal response bias, regardless of facial expression. Because of this dissociation and because the effects of facial expression and background colour did not interact, it is concluded that the angry face benefit in STM is a valence and not an arousal effect. *

Corresponding author S. Langeslag is now at: Erasmus MC – Sophia Children‘s Hospital, Department of Child & Adolescent Psychiatry, P.O. Box 2060, NL-3000 CB Rotterdam, The Netherlands, E-mail address: [email protected]. Tel: +31 (0)10 703 7071. Fax: +31 (0)10 703 2111.

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Sandra J. E. Langeslag, Margaret C. Jackson, Jan W. van Strien et al.

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It is suggested that these stimulus valence and contextual arousal effects have different underlying mechanisms.

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Chapter 177

WORKING MEMORY DEFICITS IN SCHIZOPHRENIA: NEUROBIOLOGICAL CORRELATES AND TREATMENT Haiyun Xu1,2, Hong-Ju Yang1and Gregory M. Rose1,2 1

Department of Anatomy, 2 Center for Integrated Research in Cognitive and Neural Sciences, School of Medicine, Southern Illinois University Carbondale, Carbondale, IL, US

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Working memory is a cognitive process dedicated to the transitory maintenance and online manipulation of information. Patients with schizophrenia, a heterogeneous brain disease, show several types of working memory deficits, including in visuospatial working memory, phonological working memory, and executive functioning. These deficits may underlie other schizophrenia symptoms and predict patient outcomes. Furthermore, there is increasing evidence suggesting that working memory deficits may provide a behavioral marker of genetic liability for schizophrenia. While the dominant role of the prefrontal dysfunction in working memory deficits of patients with schizophrenia has been appreciated, there is increasing evidence suggesting the existence of disturbed functional connectivity within brain networks subserving domain-specific components of working memory in schizophrenia. This functional deficit may result from dysfunctional neurotransmitter systems, of which the dopaminergic system has been best characterized, and/or white matter abnormalities which have been shown to be a consistent pathological finding in brains of schizophrenia patients. Working memory deficits in schizophrenia can be somewhat relieved by antipsychotics and various cognitive rehabilitation approaches. Atypical, but not typical, antipsychotics have shown some promise for relieving working memory deficits in patients with schizophrenia. Cognitive rehabilitation, an alternative to pharmacological treatment of cognitive deficits in patients with schizophrenia, also shows promise, but further work needs to be done to optimize this approach. Developing effective treatments for working memory impairments in schizophrenia patients remains an important therapeutic goal.

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Chapter 178

TOBACCO, NICOTINE AND COTININE: FOR MEMORY, NEUROLOGICAL, AND PSYCHIATRIC DISORDERS V. Echeverria1,2, P. Rajeev3 and R. Zeitlin1 1

Research and Development, Department of Veterans Affairs, Bay Pines VA Healthcare System, Bay Pines, FL, US 2 Department of Molecular Medicine, University of South Florida, Tampa, FL, US 3 Department of Chemistry, University of Miami, FL, US

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RESEARCH SUMMARY Epidemiological studies have associated tobacco consumption with a lower incidence of Alzheimer‘s disease (AD) and Parkinson‘s disease (PD). The neuroprotective effect of tobacco has been mainly attributed to the stimulation by nicotine of the 7 nicotinic acetylcholine receptors (nAChRs), which are implicated in neuronal survival, attention, and memory. A reduction in cholinergic function including lower levels of the expression of nAChRs in the hippocampus correlates with memory impairment in AD and schizophrenia. Although nicotine improves memory, sensory gating, and attention, its toxicity and undesired effects such as negative cardiovascular effects have terminated its therapeutic applications. Interestingly, its main metabolite cotinine shows similar neuroprotective and mnemonic properties but has a ten-fold longer half-life than nicotine and a good safety profile in humans. In neurodegenerative conditions including AD and PD, the accumulation of aggregated forms of the -amyloid peptide correlates with cognitive impairment. Cotinine has been shown to reduce A aggregation in vitro. Additionally, since cotinine is a weak agonist of the nAChRs, we postulate that cotinine improves neuronal survival and memory at least in part by acting as a positive modulator of the 7 nAChRs. The potentiation of 7 nAChRs by cotinine can be beneficial in a broad range of neurological disorders such as schizophrenia, AD, attention-deficit hyperactivity disorder, and PD in which the modulation of these receptors can ameliorate working memory and attention. Based on actual evidence and these ideas, the relevance and potential therapeutic use of cotinine in several neurological disorders are discussed in this chapter.

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Chapter 179

WORKING MEMORY AND FUNCTIONAL OUTCOME IN PATIENTS WITH MAJOR DEPRESSIVE DISORDER Yasuhiro Kaneda* Department of Psychiatry, Iwaki Clinic, Tokushima, Japan

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RESEARCH SUMMARY Objective: Patients with major depressive disorder (MDD) have been reported to perform less well in neurocognitive tests than normal control subjects. The author tested the hypotheses that a specific type of cognitive function, namely verbal working memory (WM), in patients with MDD is predictive of the functional outcome. Study 1: In this naturalistic cross-sectional study, the subjects consisted of 54 clinic adult out-patients. The assessments were performed using the 7-item Hamilton Rating Scale for Depression (HAM-D7) for the severity of depression, and the Digit Sequencing Task (DST) for evaluation of verbal WM. Functional outcome was rated on a scale of 0 (non-impaired) to 3 (severely impaired). The author found that, in the patients with current episode of MDD, functional outcome was significantly correlated with HAM-D7 scores, but not with DST scores. Meanwhile, in a sample of full remitted or partial remitted (mildly depressed) patients, functional outcome was significantly correlated with both DST and HAM-D7 scores. Moreover, in a sample of full remitted or partial remitted (mildly depressed) patients, the DST scores significantly contributed to the prediction of the functional outcome, but the HAMD7scores did not.

*

Corresponding author: Yasuhiro Kaneda, M.D., Ph.D., Dept. of Psychiatry, Iwaki Clinic, 11-1 Kamimizuta, Gakubara, Anan, Tokushima 774-0014, Japan. Tel: +81-884-23-5600. Fax: +81-884-22-1780, E-mail: [email protected].

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Yasuhiro Kaneda

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Study 2: In this naturalistic longitudinal study, the subjects consisted of 24 adult outpatients. Significant decrease of the HAM-D7 scores was observed during the 12-week study period, whereas the DST scores showed no significant increase. At base-line, the functional outcome was significantly correlated with the scores on HAM-D7, but, at 12 weeks, it was significantly correlated with both HAM-D7 and DST scores. According to a multiple regression analysis, the DST scores at baseline significantly contributed to prediction of the functional outcome at 12 weeks. Conclusion: These studies suggest the existence of a correlation between a deficit of verbal WM and the functional outcome after treatment in patients with MDD. Enhancement of verbal WM function may be useful to achieve normalization of functioning as an important component of remission in addition to symptomatic remission.

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Chapter 180

CONTROL OF WORKING MEMORY CONTENTS DURING TASK-SWITCHING James A. Grange*

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

Centre for Cognitive Neuroscience, Bangor University, Bangor, Gwynedd, UK

RESEARCH SUMMARY Every day life requires frequent switches between tasks in order to achieve goal- directed behaviour. For example, driving presents us with a complicated environment wherein many sub-tasks---speed monitoring, steering, recollection of directions from memory etc.---must be switched between in order to arrive safely at our destination. However, as working memory is limited in capacity, the question arises as to how a new task is implemented in working memory in the face of conflicting activation from the now-irrelevant task. The mechanisms that allow such fluid switching are measured by utilising the so- called task-switching paradigm. Within this paradigm, participants switch between two or three simple cognitive tasks (e.g. odd/even; higher/lower than 5 judgements on number stimuli). Recent research from the task-switching paradigm has suggested that task performance is afforded by activation of task-relevant representations in working memory. Such an established representation guides behaviour by directing attention to task-relevant stimuli and actions whilst filtering out task-irrelevant information. The present chapter provides a critical review of behavioural results in the taskswitching paradigm, outlining the controversies that have surrounded this popular paradigm in recent years. This chapter also reviews the concept of inhibitory mech- anisms in task-switching, serving to suppress the activation levels of the previously relevant task. Inhibition is inferred by slower reaction times returning to a recently executed task after one intervening trial (an ABA sequence) compared to returning to a task not recently executed (a CBA sequence, where A, B, & C are arbitrary labels for tasks). This reaction time cost is thus an important phenomenon for exploring the dynamics of inhibitory processes of working memory contents during task-switching. *

Please address all correspondence to James A. Grange, who is now at Keele University, School of Psychology, Dorothy Hodgkin Building, Keele University, Keele, Staffordshire, UK (email: [email protected].

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Chapter 181

DEVELOPMENT OF NEURAL MECHANISMS OF WORKING MEMORY V. Vuontela1 and S. Carlson1,2,3 1

Neuroscience Unit, Institute of Biomedicine/Physiology, University of Helsinki, Helsinki, Finland 2 Brain Research Unit, Low Temperature Laboratory, Aalto University School of Science and Technology, Espoo, Finland 3 Medical School, University of Tampere, Tampere, Finland

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RESEARCH SUMMARY Working memory (WM), the ability to hold and manipulate information online, improves during childhood as shown by an increase in WM capacity and a positive correlation between age and measures of WM performance. Intact function of WM is essential in many forms of complex cognition such as learning, reasoning, problem solving and language comprehension. WM function has a strong impact on academic achievement and is related to adaptive functioning at school. Children with deficits in WM have learning difficulties that are often accompanied by behavioural problems. The neural processes subserving WM performance and brain structures supporting this system continue to develop throughout childhood till adolescence and early adulthood. The prefrontal cortex (PFC), that is one of the last brain regions to mature, has a central role in the function of WM. WM network involves also distributed areas in parietal, temporal and striatal regions. It has been suggested that neuroanatomical brain development occurs in parallel with behavioural and cognitive maturation during childhood and adolescence. In this chapter, we focus on the neural mechanisms that support the function of WM, their developmental trajectories and relation of their development to the maturation of cognitive abilities.

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V. Vuontela and S. Carlson

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We will also discuss the development of the brain‘s ―default-mode‖ network that is active in the absence of cognitive task performance, i.e. during a resting state and shows attenuation of activation (deactivation) when the brain becomes engaged in attention requiring cognitive task performance. Deactivation mechanisms are important in the performance of WM tasks: inability to deactivate is associated with impaired task performance and is evident in patients with certain neuropsychological disorders.

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Chapter 182

MOLECULAR IMAGING B. Schaller and N. Sandu Department of Neurosurgery, University Hospital of Paris, France

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

RESEARCH SUMMARY Accurate anatomical localization of functional abnormalities obtained with the use of positron emission tomography (PET) is known to be problematic (1). Although tracers such as (18)F-fluorodeoxyglucose ((18)F-FDG) visualize certain normal anatomical structures, the spatial resolution is generally inadequate for accurate anatomic localization of pathology (2). Combining PET with a high-resolution anatomical imaging modality such as computed tomography (CT) can resolve the localization issue as long as the images from the two modalities are accurately coregistered. However, software-based registration techniques have difficulty accounting for differences in patient positioning and involuntary movement of internal organs, often necessitating labor-intensive nonlinear mapping that may not converge to a satisfactory result. Acquiring both CT and PET images in the same scanner obviates the need for software registration and routinely provides accurately aligned images of anatomy and function in a single scan. A CT scanner positioned in line with a PET scanner and with a common patient couch and operating console has provided a practical solution to anatomical and functional image registration. Axial translation of the couch between the 2 modalities enables both CT and PET data to be acquired during a single imaging session. In addition, the CT images can be used to generate essentially noiseless attenuation correction factors for the PET emission data. By minimizing patient movement between the CT and PET scans and accounting for the axial separation of the two modalities, accurately registered anatomical and functional images can be obtained. Since the introduction of the first PET/CT prototype more than 6 years ago, numerous patients with cancer have been scanned on commercial PET/CT devices worldwide. The commercial designs feature multidetector spiral CT and highperformance PET components.

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B. Schaller and N. Sandu

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Experience has demonstrated an increased level of accuracy and confidence in the interpretation of the combined study as compared with studies acquired separately, particularly in distinguishing pathology from normal, physiologic tracer uptake and precisely localizing abnormal foci. Combined PET/CT scanners represent an important evolution in technology that has helped to bring molecular imaging to the forefront in cancer diagnosis, staging and therapy monitoring.

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Chapter 183

MRI MEASUREMENT OF FORNIX PATHOLOGY: EVIDENCE OF EXTENSIVE FORNIX DAMAGE FOLLOWING SURGICAL REMOVAL OF COLLOID CYSTS IN THE THIRD VENTRICLE Christine E. Denby1, Seralynne D. Vann2, Dimitris Tsivilis1, John P. Aggleton2, Andrew R. Mayes1, Vanessa Sluming3, Neil Roberts4 and Daniela Montaldi1,

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1

School of Psychological Sciences, Zochonis Building, University of Manchester, Brunswick Street, Manchester, UK 2 School of Psychology, Cardiff University, Cardiff, Wales, UK 3 Division of Medical Imaging, Johnston Building, University of Liverpool, Liverpool, UK 4 Magnetic Resonance and Image Analysis Research Centre (MARIARC), Liverpool, UK

RESEARCH SUMMARY A large cohort of post-surgical colloid cyst patients (n=38) was scanned to provide MR data with which to explore two measures of fornix integrity, overall volume and smallest cross-sectional area. The 3T MRI scans, which provided the first quantitative analysis of fornix volume in this condition, were analysed using a manual segmentation technique. Comparisons were made with 20 healthy age-matched controls. First, inter-rater and intrarater reliability measures were determined for both fornix volume and cross-sectional area from a subset of 20 cases (10 patients, 10 controls). 

Send correspondance to: Dr Daniela Montaldi; School of Psychological Sciences, Zochonis Building, University of Manchester, Brunswick Street, Manchester, M13 9PL; [email protected]; Tel: 01612757335.

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Christine E. Denby, Seralynne D. Vann, Dimitris Tsivilis et al.

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The overall volume measure had acceptable levels of reliability. Subsequent volumetric analyses showed that while the large majority of colloid cyst patients did not suffer complete interruption of the tract, the colloid cyst group had significantly reduced right (368mm³) and left (398mm³) fornix volumes compared to the control volumes (right 507mm³, left 533mm³). Overall, the study revealed that incomplete fornix damage is a common feature in colloid cyst patients. This finding contrasts with the dichotomised descriptions of the fornix (intact or lost) that are more standardly provided after visual inspection of scans. Partial disconnection of the hippocampus is likely to produce long-term memory problems with implications for follow-up monitoring and treatment.

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Chapter 184

SUDDEN INTRAUTERINE UNEXPLAINED DEATH (SUD) “GRAY ZONE” OR BORDERLINE Giulia Ottaviani "Lino Rossi" Research Center for the Study and Prevention of the Unexpected Perinatal Death and SIDS, and Institute of Pediatrics and Neonatology, University of Milan, Milan, Italy

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RESEARCH SUMMARY The author reports the histopathological findings of 9 fetuses (3 females and 6 males, ranging in age from 34 to 41 gestational weeks) that died suddenly and unexpectedly in utero. They presented brainstem and cardiac conduction system lesions together with abnormalities of the fetal adnexa. A complete autopsy was performed, including detained investigation of the brainstem and cardiac conduction system on serial sections, as well as of the fetal adnexa, according to our guidelines. Histological examination of the fetal adnexa disclosed the presence of chorioamnionitis (7 cases), an abnormally short umbilical cord (1 case), and placental infection by parvovirus (1 case). These lesions were associated with brainstem lesions, i.e., hypoplasia of the arcuate nucleus (6 cases), inflammatory infiltrates in the brainstem (2 cases), hypoplasia of the raphe obscurus nucleus (2 cases), hypoplasia of the parabrachial Kölliker-Fuse complex (1 case), hypoplasia of the pre-Bötzinger complex (1 case), agenesis of the facial/parafacial complex (1 case), as well as conduction system lesions, i.e., dispersion or septation of the atrio-ventricular junction (9 cases), islands of the conduction system inside the central fibrous body (5 cases) resorptive degeneration (4 cases), cartilaginous meta-hyperplasia (2 cases), Mahaim fibers (1 case). Each SIUD victim presented at least one of these brainstem and/or cardiac conduction abnormalities, more than one change being present in the same fetus.



Send correspondance to: Giulia Ottaviani, M.D.; Institute of Pediatrics and Neonatology, University of Milan, Via della Commenda, 9, 20122 Milan, Italy; Tel. +39-02-50320822; Fax: +39-02-50320823; E-mail: [email protected]; URL: http://users.unimi.it/giuliaottaviani/

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Giulia Ottaviani

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The SIUD «gray zone», or borderline cases, are hereby described as those cases in which the lesions of the fetal adnexa alone might not have accounted for the sudden deaths, had it not been for the concomitant presence of brainstem and cardiac conduction lesions representing the morphological substrates for SIUD, as well as for SIDS. Our 9 cases are consistent with the triple-risk model, a hypothesis introduced for SIDS postulating an underlying biological vulnerability to exogenous stressors or triggering factors in a critical developmental period. In conclusion, we are convinced that there is a continuum between SIUD and SIDS and the triple-risk model is herein considered for the first time also for SIUD ―gray zone‖ victims.

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Chapter 185

NEUROIMAGING OF THE FORNIX: PRESENT AND FUTURE Christine E. Denby1,, Seralynne D. Vann2, Dimitris Tsivilis1, Andrew R. Mayes1, Daniela Montaldi1 and John P. Aggleton2 1

School of Psychological Sciences, Zochonis Building, University of Manchester, Brunswick Street, Manchester, UK 2 School of Psychology, Cardiff University, Park Place, Cardiff, Wales, UK

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RESEARCH SUMMARY The fornix is a major white matter tract that is critical for normal memory. Structural magnetic resonance imaging has been employed as a tool for investigating fornix integrity since 1988, when it was first used to link fornix damage to changes in cognition. However, there are still relatively few reports of magnetic resonance imaging (MRI) studies of the fornix, with even fewer studies attempting to provide volumetric estimates of the structure. The fornix is anatomically complex in nature, with its curvature proving a challenge for volumetric analysis. Successful qualitative, and in some cases, quantitative MRI studies examining the integrity of the fornix have been performed in the following patient groups; temporal lobe epilepsy, colloid cyst, schizophrenia, and traumatic brain injury. This review details the current fornix neuroimaging literature, including the anatomy and quantitative methodology used to acquire volume estimates. We also explore new developments in MRI methodology, which will shape the future of fornix neuroimaging.



Send correspondance to: Dr. Christine Denby; School of Psychological Sciences, Zochonis Building, University of Manchester, Brunswick Street, Manchester, M13 9PL; Email: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

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In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 186

HIGH-FIELD MR IMAGING IN NEUROSCIENCE RESEARCH N. R. Jagannathan Dept. of NMR, All India Institute of Medical Sciences, New Delhi, India

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RESEARCH SUMMARY The growth of human intellect over many centuries is borne out of myriad of experiences. The challenges in the development of magnetic resonance imaging and spectroscopy technology is one such example wherein the quest is to achieve superior image quality with high resolution and high signal-to-noise ratio (SNR) for early detection of diseases and to study the metabolic processes. The development of clinical MR scanners from low to high field (≥ 3 T) has been continuous and educative. In the early days of MRI, there were doubts whether MRI scanners would go beyond the1 Tesla limit. Presently number of high field 3.0 T MRI systems is installed worldwide and several studies report the comparison of MR imaging carried out on brain and whole body applications at 1.5 T and 3.0 T. While SNR is advantageous at high fields, the increased RF absorption in tissues is undesirable. Based on the clinical requirement and the situation, the advantage of high field MR imaging is governed by the use of appropriate pulse sequence, the parameters used and how efficiently the artifacts are eliminated or compensated. Even though the SNR increases linearly with the increasing magnetic field, longer T1, susceptibility and the dielectric effects reduce the achievable SNR. Additionally, the acquisition strategies used may also reduce the SNR advantage gained. Thus in most clinical situations, the net SNR gain for example, at 3T will be less than two compared with 1.5T. Another aspect apart from the increase in SNR is the need and sufficient evidence for use of high field-strength MR for clinical purposes.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 187

PERIOPERATIVE ATRIAL FIBRILLATION AND THE RISK OF STROKE Maciej Banach and Jacek Rysz Department of Molecular Cardionephrology and Hypertension, Medical University of Lodz, Poland, Zeromskiego, Lodz, Poland Department of Nephrology, Hypertension and Family Medicine, Medical University of Lodz, Poland

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RESEARCH SUMMARY The prevalence of atrial fibrillation (AF) has been still increased in the ageing population. In the UK, the occurrence of AF has risen from 0.78% in 1994 to 1.42% in 2006. The similar prevalence is observed in the Central European countries. The incidence of age- and genderadjusted AF rose from 3.04 to 3.89 per 1000 person-years, between 1980 and 2006. As a result of recent developments in invasive cardiology together with much improved methods of pharmacological treatments, cardiac surgeons are increasingly operating on elderly patients with very advanced heart disease and many other coexistent diseases. Therefore, AF is often present before cardiac surgery, increasing the risk of surgery and the occurrence of postoperative complications.



E-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 188

MINI-REVIEW: ETHICS IN NEUROSCIENCE Bernhard Schaller Department of Neurosurgery, University of Paris, France

RESEARCH SUMMARY

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved.

The ethical implications of the many rapid advances in neuroscience continue to feed the growth of neuroethics, which is taking an increasingly prominent place in the larger field of bioethics. Four main developments have stirred discussion and debate in neuroethics this past year: (i) commercialization of lie detection, (ii) proposals to use deep brain stimulation for treating depression, (iii) advances in the genetic understanding of addiction, and (iv) improvements in brain imaging for diagnostic purposes.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 189

THE FUNCTIONAL NEUROIMAGING OF THE PRECUNEUS Andrea E. Cavanna1,2, Luca Bertero3 and Stefano L. Cavanna3 1

2

Institute of Neurology, London, United Kingdom Department of Neurology, Amedeo Avogadro University, Novara, Italy 3 University of Turin Medical School, Turin, Italy

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RESEARCH SUMMARY Over the last few years functional neuroimaging studies have started unravelling unexpected functional attributes for the precuneus, a previously neglected area located in the posteromedial parietal cortex. Multiple sources of evidence from fMRI and PET investigations suggest a central role for the precuneus in a wide spectrum of highly integrated tasks, including visuo-spatial imagery, episodic memory retrieval, and self-processing operations, namely first-person perspective taking and an experience of agency. Furthermore, the precuneus and surrounding structures within the posteromedial parietal region are thought to represent a crucial node in the ‗default mode‘ system, a network of brain structures displaying high resting metabolic rate and transient deactivations during engagement in non self-referential tasks. Therefore, it has recently been proposed that the precuneus plays a pivotal role in the neural correlates of consciousness, engaged in self-related mental representations during rest. This hypothesis is consistent with the selective hypometabolism in the posteromedial cortex reported in a wide range of pathophysiological states characterised by altered consciousness, such as sleep, vegetative state, and pharmacological anaesthesia. Functional neuroimaging studies on neuropsychiatric populations showing disruption of the ‗default mode‘ activity have recently added novel insights into the understanding of the behavioural correlates of the precuneus.



Correspondence to: Andrea Eugenio Cavanna, MD. Institute of Neurology, Queen Square, London WC1N3BG, UK. E-mail: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 190

LINK BETWEEN BASIC AND CLINICAL RESEARCH BY FUNCTIONAL IMAGING Bernhard J. Schaller Skull Base Institute,Germany

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RESEARCH SUMMARY The human mind commands our attention. We are justly fascinated by the workings of our own mind and of others. We should be; all of our culture reveals the luxuriant complexities of the mind. Studies of the mind from neuroscience and psychiatry have risen to the richness of the subject with brilliant descriptions of mental phenomena and insights into mechanisms. It is not surprising, therefore, that scientific studies of the mind start with observations of brain responses during mental activities in an effort to explore down to a level where, as Francis Crick urged us, "our minds—the behavior of our brains—can be explained by the interactions of nerve cells (and other cells) and the molecules associated with them". Much of recent optimism about being able to bridge the brain and the mind derives from functional positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). These methods are often represented as directly mapping neuronal activity in the functioning human brain. Impressive two- and three-dimensional maps of "neuronal activity" in the functioning brain have been embraced by scientists and the popular media as providing new insights into the biological basis of how the mind works. In functional imaging studies of sensory perception, recent progress is heartening, with impressive identifications and localizations of sensory functions, such as color or edge detection in the extra striate cortex. When we combine the results of these studies on humans with electrophysiological and cellular studies of animal models, we gain important insights into how complex sensory functions are supported by the brain‘s molecular and cellular activity. But when functional imaging studies have approached conceptual activities of the mind, progress has taken on a different complexion. Functional imaging studies of mental processes are interpreted almost exclusively within an established paradigmatic view of "mind"—an interpretation that exposes both the strengths and limitations of the methods.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 191

EXTENDED EXPRESSION FOR TRANSVERSE MAGNETIZATION USING FOUR PULSE SEQUENCE TO CONSTRUCT DOUBLE QUANTUM FILTER OF ARBITRARY PHASES FOR SPIN 3/2 SODIUM NUCLEI Rakesh Sharma Department of Medicine and Radiology, Columbia University of Health Sciences, New York, NY, US

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RESEARCH SUMMARY The extended expression for the transverse magnetization for the standard sodium MRI four pulse sequence employed in the construction of a double-quantum filter is derived for arbitrary phase angles. By use of the extended expression the NMR signal intensity of the corresponding double-quantum filter was maximized when the phases and phase cycling of the pulses employed were determined accordance with the coherence-transfer pathway formalism. Furthermore, the filtering action of the double-quantum filter was insensitive to perturbations in the phase angles of up to ± 5° around the values. For these variations in phase angles, the transverse magnetization of the double-quantum filter signal decreases by less than 5%. This decrease in signal intensity was due to the function dependence of the transverse magnetization on the phase angles. The pulse sequence specific to double quantum filter is described useful in design of clinical sodium MRI technique.



Corresponding Address: Rakesh Sharma, Ph.D. Departments of Medicine and Radiology, PH 10th Floor, Room 409, College of Physicians and Surgeons, 630, West 168th Street, New York, NY 10032. Phone: (212)305 9008 (Office); (212)305 8759; Email: [email protected].

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 192

MALDI IMAGING: A REVIEW OF THE CURRENT STATUS OF THE TECHNOLOGY Isabelle Fournier1, Franck Julien1, Maxence Wisztorski1, Eduardo Macagno2 and Michel Salzet1 1

University of Lille1, équipe Imagerie MALDI, Laboratoire de Neuroimmunologie des Annélides 2 Section of Cell and Developmental Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, California, US

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RESEARCH SUMMARY Biological systems are heterogeneous ensembles whose complex molecular composition makes them inherently difficult to analyze. A critical first step is the identification and characterization of their molecular components, particularly peptides and proteins, a task that has been enormously facilitated by the development of mass spectrometry (MS) into the powerful and versatile technology it is today. The increasing capacity of MS to measure molecular weights with high precision and to provide primary and, more recently, secondary structural information, makes this the technique of choice for analyzing complex biomolecular mixtures. However, the identification of the molecular constituents, while of primary importance, is not sufficient for understanding their functions in a biological context, for which acquiring knowledge of their distributions (locations and abundances) is an essential next step. This dimension is now possible by performing mass spectrometry imaging (MSI), especially Matrix Assisted Laser Desorption/Ionisation Mass Spectrometry Imaging (MALDI Imaging) directly on tissue slices. After some ten years of important technical developments, MALDI-MS appears to be a sufficiently mature technology to be introduced in laboratories as the best approach to exploring tissue properties at the molecular level, particularly in the comparison of normal versus pathological states to study the nature of neurological diseases. In this report, we will discuss the advantages and current limitations of this technique.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

Copyright © 2012. Nova Science Publishers, Incorporated. All rights reserved. Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova

In: Neuroscience Researcher Biographical Sketches ... ISBN 978-1-62100-943-6 Editors: A. A. Chernyovskaya and G. F. Klossovsky © 2013 Nova Science Publishers, Inc.

Chapter 193

IMAGING IN MOLECULAR DYNAMICS: TECHNOLOGY AND APPLICATIONS Benjamin Whitaker Cambridge University Press, New York, US

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RESEARCH SUMMARY The experimental technique of charged-particle imaging as applied to the study of molecular reaction dynamics is the subject of Imaging in Molecular Dynamics, edited by Benjamin Whitaker. The book—consisting of 11 chapters, each written by various contributors—is organized into two parts: Technology and Applications. Chapters 2 and 3, ―Velocity Map Imaging‖ and ―Reconstruction Methods,‖ constitute about a third of the book. These two chapters lay out the background theory and practice of obtaining product data from molecular reactions by directly imaging the ―Newton sphere‖ produced by a molecular reaction. The rest of the first part describes different experimental variations of the basic technique and includes chapters on time-resolved measurements, obtaining three-dimensional velocity information, and the use of femtosecond lasers to probe subpicosecond reaction dynamics. The second part of the book, Applications, contains three chapters covering specific research applications and a fourth on a new approach to velocity map imaging. The three specific examples were chosen to display the breadth of applications available: coincidence imaging and the study of bimolecular collisions. The final chapter of the book presents a version of velocity map imaging, which resembles confocal imaging.

Neuroscience Researcher Biographical Sketches and Research Summaries, edited by Abram A. Chernyovskaya, and Graviil F. Klossovsky, Nova