Verhaagen / Hol / Huitinga Neurotherapy

Progress in Restorative Neuroscience and Neurology
1. Auflage 2009
ISBN: 978-0-08-092296-6
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 414 Seiten

This book focuses on the exciting recent progress in restorative neurology and neuroscience. The book includes chapters on major neurodegenerative disorders of the brain and the visual system, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, macular degeneration, retinitis pigmentosa, glaucoma, spinal cord trauma, and multiple sclerosis. The primary goal of the book is to give an overview of new developments in translational research and in potential therapeutic strategies, including stem cell therapy, immunotherapy, gene therapy, pharmacotherapy, neuroprostheses and deep brain stimulation.
* Provides the reader with a unique overview over all aspects of new advances in the therapy of neurological and psychiatric disorders
* Covers all levels of biological organization including novel molecular and cellular targets, electrophysiological, anatomical and behavioural substrates of neurodegeneration and the application of whole brain in vivo imaging
* Broad focus with contributions by the top scientists worldwide in the respective disciplines

Autoren/Hrsg.

Verhaagen, Joost

Hol, Elly M.

Huitinga, Inge

Wijnholds, Jan

Bergen, Arthur B.

Boer, Gerard J.

Swaab, Dick F.

Inhaltsverzeichnis

1;Front cover;1
2;Neurotherapy: Progress in Restorative Neuroscience and Neurology;4
3;Copyright page;5
4;List of Contributors;6
5;Preface;10
6;Acknowledgments;12
7;Contents;14
8;Section I. Stem Cells;18
8.1;Chapter 1. Cell transplantation strategies for retinal repair;20
8.1.1;Therapeutic strategies to restore the neural retina;20
8.1.2;Cell sources for retinal transplantation;23
8.1.3;Optimization of transplanted cell integration;27
8.1.4;Future considerations for retinal cell therapy;31
8.1.5;Abbreviations;32
8.1.6;Acknowledgments;32
8.1.7;References;32
8.2;Chapter 2. Strategies for retinal repair: cell replacement and regeneration;40
8.2.1;The retina and its degenerations;40
8.2.2;Retinal developmental biology;41
8.2.3;The ciliary marginal zone;41
8.2.4;Endogenous retinal repair mechanisms: Müller glia as a source of new neurons;42
8.2.5;Cell replacement strategies for retinal repair;44
8.2.6;Concluding remarks;46
8.2.7;References;47
8.3;Chapter 3. The rostral migratory stream and olfactory system: smell, disease and slippery cells;50
8.3.1;The purpose and importance of olfaction;50
8.3.2;The rostral migratory stream (RMS) pathway: common anatomical features in vertebrates;52
8.3.3;Polysialylated neural cell adhesion molecule: making the neuroblast slippery;54
8.3.4;The fate determinants for neuroblasts arriving at the olfactory bulb;56
8.3.5;Could the RMS be exploited for treating brain disordersquest;56
8.3.6;References;57
8.4;Chapter 4. Identifying and enumerating neural stem cells: application to aging and cancer;60
8.4.1;Neural stem cell discovery;60
8.4.2;Identifying neural stem cells using the neurosphere assay (NSA);61
8.4.3;Enumeration of neural stem cells using the neural-colony forming cell assay and a mathematical model;61
8.4.4;Neural stem cells: potential treatment for age-related CNS disorders;62
8.4.5;Neural stem cells and brain tumors;64
8.4.6;Conclusion;65
8.4.7;References;66
8.5;Chapter 5. Transgenic reporter mice as tools for studies of transplantability and connectivity of dopamine neuron precursors in fetal tissue grafts;70
8.5.1;Introduction;70
8.5.2;Cell therapy for Parkinson’s disease;71
8.5.3;Midbrain dopamine neurons;74
8.5.4;Isolation of transplantable midbrain dopamine neurons from stem cell-derived populations;75
8.5.5;Reporter mice as tools in neural transplantation studies;78
8.5.6;Isolation of midbrain dopamine neuronal precursors from the developing midbrain;78
8.5.7;Graft composition and its relevance for functional impact;82
8.5.8;Reconstruction of the nigro-striatal pathway through intra-nigral grafting;86
8.5.9;Concluding remarks;91
8.5.10;References;91
9;Section II. Immunotherapy and Vaccination Therapy;98
9.1;Chapter 6. Developing novel immunogens for a safe and effective Alzheimer’s disease vaccine;100
9.1.1;Introduction;101
9.1.2;Abeta immunotherapy in rodents, monkeys, and humans;101
9.1.3;Novel short Abeta immunogens for active vaccination;105
9.1.4;Conclusions;107
9.1.5;Acknowedgments;108
9.1.6;References;108
9.2;Chapter 7. Innate immunity in the nervous system;112
9.2.1;The complement system;112
9.2.2;Activation and regulation of the complement system;113
9.2.3;The role of complement in inflammation;114
9.2.4;Complement in the central nervous system (CNS);114
9.2.5;Complement in the peripheral nervous system (PNS);120
9.2.6;Complement regulation in nerve injury and disease: a therapeutic approach;130
9.2.7;Abbreviations;132
9.2.8;Acknowledgment;133
9.2.9;References;133
9.3;Chapter 8. Neuroinflammation in spinal cord injury: therapeutic targets for neuroprotection and regeneration;142
9.3.1;Introduction to spinal cord injury (SCI) pathology: neuroinflammation in the pathogenesis of secondary injury;142
9.3.2;Manipulating neuroinflammation to improve recovery from SCI;143
9.3.3;Consequences of neuroinflammation on neuronal plasticity and regeneration;146
9.3.4;Conclusions;148
9.3.5;Acknowledgments;148
9.3.6;References;148
9.4;Chapter 9. Toll-like receptors in the CNS: implications for neurodegeneration and repair;156
9.4.1;Introduction and scope of this chapter;156
9.4.2;General features of TLRs;157
9.4.3;Expression and function of TLRs in microglia;158
9.4.4;Expression and function of TLRs in astrocytes;159
9.4.5;Expression and function of TLRs in neurons;162
9.4.6;Concluding remarks and future perspectives;163
9.4.7;Abbreviations;163
9.4.8;Acknowledgements;163
9.4.9;References;163
10;Section III. Gene Therapy;166
10.1;Chapter 10. Gene therapy and transplantation in the retinofugal pathway;168
10.1.1;Introduction;169
10.1.2;AAV-mediated transduction of retinal ganglion cells;169
10.1.3;Use of LV to genetically modify Schwann cells in chimeric peripheral nerve grafts;171
10.1.4;Transduction and tropic properties of modified AAV vectors in the retina;171
10.1.5;Concluding comments;175
10.1.6;References;175
10.2;Chapter 11. Controlled dissemination of AAV vectors in the primate brain;180
10.2.1;Introduction;180
10.2.2;Trafficking of AAV in the brain;181
10.2.3;Real-time imaging;184
10.2.4;Clinical implications;185
10.2.5;Conclusion;187
10.2.6;References;187
10.3;Chapter 12. From microsurgery to nanosurgery: how viral vectors may help repair the peripheral nerve;190
10.3.1;Introduction: peripheral nerve repair;190
10.3.2;Molecular mechanisms involved in peripheral nerve regeneration;191
10.3.3;Current challenges in peripheral nerve repair;192
10.3.4;Viral vectors: promising tools to express potentially therapeutic proteins in injured peripheral nerves;194
10.3.5;Lentiviral vector-mediated overexpression of neurotrophic factors to enhance nerve regeneration;195
10.3.6;Enhancing motoneuron survival as an application of neurotrophic factors;198
10.3.7;Failed functional recovery: misrouting of regenerating axons is an important factor;198
10.3.8;Addressing the routing problem at a molecular level;199
10.3.9;Future perspective: the continuing miniaturization of surgical and diagnostic tools;200
10.3.10;References;201
10.4;Chapter 13. Gene therapy for neurodegenerative diseases based on lentiviral vectors;204
10.4.1;Lentiviral vector-mediated gene therapy;204
10.4.2;Amyotrophic lateral sclerosis;206
10.4.3;Spinal muscular atrophy;207
10.4.4;Parkinson’s disease;208
10.4.5;Huntington’s disease;210
10.4.6;Clinical prospects and challenges of lentiviral vectors;212
10.4.7;Abbreviations;212
10.4.8;References;213
10.5;Chapter 14. Trophic factors therapy in Parkinson’s disease;218
10.5.1;Parkinson’s disease and neurotrophic factors;218
10.5.2;Glial cell line-derived neurotrophic factor;219
10.5.3;Neurturin;227
10.5.4;References;232
11;Section IV. Pharmacotherapy;234
11.1;Chapter 15. Progesterone as a neuroprotective factor in traumatic and ischemic brain injury;236
11.1.1;Introduction;236
11.1.2;Stroke and progesterone;239
11.1.3;Conclusion;249
11.1.4;Abbreviations;250
11.1.5;Acknowledgment;250
11.1.6;References;250
11.2;Chapter 16. Estrogen and testosterone therapies in multiple sclerosis;256
11.2.1;Introduction;256
11.2.2;Potential mechanisms of sex hormones;259
11.2.3;Sex hormone treatments in MS;262
11.2.4;Conclusions and future directions;263
11.2.5;Abbreviations;264
11.2.6;Acknowledgments;264
11.2.7;References;264
11.3;Chapter 17. Treatment of retinal diseases with VEGF antagonists;270
11.3.1;Introduction;270
11.3.2;Ocular angiogenesis;270
11.3.3;Mechanisms of angiogenesis and wound healing;271
11.3.4;Role of VEGF in ocular pathology and clinical use of VEGF antagonists;274
11.3.5;VEGF antagonists in AMD and other conditions with subretinal neovascularization;279
11.3.6;Side effects of ocular use of VEGF antagonists;280
11.3.7;Conclusion;281
11.3.8;References;281
11.4;Chapter 18. Pharmacological modification of the extracellular matrix to promote regeneration of the injured brain and spinal cord;286
11.4.1;Introduction;286
11.4.2;Lesion scarring after CNS injury;287
11.4.3;Differences in axonal growth responses to scar formation;289
11.4.4;Therapies to prevent fibrous scar formation;290
11.4.5;Pharmacological inhibition of scarring with iron chelators;291
11.4.6;Conclusion;295
11.4.7;Abbreviations;295
11.4.8;Acknowledgments;296
11.4.9;References;296
11.5;Chapter 19. The placebo response: neurobiological and clinical issues of neurological relevance;300
11.5.1;Introduction;300
11.5.2;Two different meanings of the term ‘‘placebo effect’’;301
11.5.3;Evolution of the sugar pill;301
11.5.4;The placebo response: reflex or cognitivequest;302
11.5.5;Neurological disorders showing prominent placebo effects;303
11.5.6;From research to clinical practice;307
11.5.7;Conclusions;307
11.5.8;Acknowledgment;308
11.5.9;References;308
12;Section V. Neuroprostheses;312
12.1;Chapter 20. Brain-computer interfaces: an overview of the hardware to record neural signals from the cortex;314
12.1.1;Introduction to neuroprostheses;314
12.1.2;Classification of BCI;317
12.1.3;Epicortical electrodes for class II BCI;319
12.1.4;Intracortical electrodes for class III BCI;323
12.1.5;References;330
12.2;Chapter 21. Artificial vision: needs, functioning, and testing of a retinal electronic prosthesis;334
12.2.1;Retinal degenerative diseases: an overview;335
12.2.2;Prospects for therapies available to RD patients;336
12.2.3;Electron prosthetic devices: general considerations;337
12.2.4;Morphological and neuronal bases for implantation of a retinal prosthesis;340
12.2.5;Central connections in retinal degeneration and prosthesis implantation;340
12.2.6;Visual perception: measurements in low vision and brain processing after therapeutic intervention;341
12.2.7;A clinical trial and testing of an epiretinal prosthetic device;343
12.2.8;References;347
12.3;Chapter 22. Progress in restoration of hearing with the auditory brainstem implant;350
12.3.1;Introduction;350
12.3.2;Cochlear implants;351
12.3.3;Brainstem implants;351
12.3.4;Conclusions;359
12.3.5;References;360
12.4;Chapter 23. Microstimulation of visual cortex to restore vision;364
12.4.1;Introduction;365
12.4.2;Microstimulation of V1 elicits saccadic eye movements;368
12.4.3;Microstimulation of V1 delays the execution of visually guided saccades;373
12.4.4;Microstimulation of V1 elicits a detection response;376
12.4.5;Can microstimulation of V1 evoke phosphenes exhibiting featuresquest;378
12.4.6;Effects of blindness on phosphene induction;379
12.4.7;Discussion;381
12.4.8;Conclusions;386
12.4.9;Abbreviations;386
12.4.10;Acknowledgment;386
12.4.11;References;386
13;Section VI. Deep Brain Stimulation, FES and TMS;394
13.1;Chapter 24. Functional neurosurgery for movement disorders: a historical perspective;396
13.1.1;Introduction;397
13.1.2;Therapy for movement disorders: a random walk around a logical thread;397
13.1.3;What is the current status of the efficiency of high-frequency stimulation in various nuclei in different diseasesquest;400
13.1.4;Deep brain stimulation: a preferred tool in functional neurosurgeryquest;403
13.1.5;What did we learn from the practice of deep brain stimulation in human patientsquest;404
13.1.6;Conclusions;406
13.1.7;References;406
13.2;Chapter 25. Recovery of control of posture and locomotion after a spinal cord injury: solutions staring us in the face;410
13.2.1;Why does spinal cord injury result in a loss of movement controlquest;411
13.2.2;Initiating, sustaining, and stopping movements: sources of control;412
13.2.3;Treatment paradigms for preserving muscle function after a spinal cord injury;414
13.2.4;Significance of the concept of ‘‘physiological state’’ of the spinal circuitry in relearning to step;418
13.2.5;Treatment paradigms for restoring locomotor control after a spinal cord injury;419
13.2.6;Integrating neuroengineering and biological concepts to regain posture and locomotion;427
13.2.7;Acknowledgments;430
13.2.8;References;406
13.3;Chapter 26. Deep brain stimulation in obsessive-compulsive disorder;436
13.3.1;Introduction;436
13.3.2;Obsessive-compulsive disorder;438
13.3.3;Clinical efficacy of DBS in OCD;438
13.3.4;Side effects of DBS in OCD;441
13.3.5;Conclusion and future;443
13.3.6;References;444
13.4;Chapter 27. The use of repetitive transcranial magnetic stimulation (rTMS) for the treatment of spasticity;446
13.4.1;Introduction;446
13.4.2;Pathophysiology of spasticity;447
13.4.3;Effects of rTMS on cortical excitability;450
13.4.4;Effects of rTMS on spinal excitability;450
13.4.5;Effects of rTMS in patients with spasticity;451
13.4.6;Conclusions;453
13.4.7;Abbreviations;454
13.4.8;References;454
14;Section VII. Mechanisms of Spontaneous Plasticity and Regeneration;458
14.1;Chapter 28. Calcium signaling and the development of specific neuronal connections;460
14.1.1;Introduction;460
14.1.2;Axonal growth cone navigation;461
14.1.3;Conclusion;466
14.1.4;Acknowledgments;468
14.1.5;References;468
14.2;Chapter 29. Remyelination in multiple sclerosis;470
14.2.1;Introduction;470
14.2.2;Demyelinated MS lesions with persistence of cells of the oligodendrocyte lineage;472
14.2.3;Lesions with oligodendroglial depopulation;473
14.2.4;Conclusion;478
14.2.5;Acknowledgments;478
14.2.6;References;478
14.3;Chapter 30. Magnetic resonance techniques to quantify tissue damage, tissue repair, and functional cortical reorganization in multiple sclerosis;482
14.3.1;Introduction;483
14.3.2;Imaging brain atrophy;483
14.3.3;Intrinsic lesion damage;484
14.3.4;Imaging ‘‘diffuse’’ normal-appearing brain tissue (NABT) and normal-appearing WM (NAWM) damage;485
14.3.5;Imaging ‘‘diffuse’’ GM damage;487
14.3.6;Cortical reorganization;488
14.3.7;Imaging the spinal cord;490
14.3.8;Imaging the optic nerve;492
14.3.9;Conclusions;492
14.3.10;References;493
14.4;Chapter 31. MRI of neuronal network structure, function, and plasticity;500
14.4.1;Introduction;500
14.4.2;Diffusion tensor imaging;501
14.4.3;Resting state fMRI;504
14.4.4;Discussion;508
14.4.5;Abbreviations;508
14.4.6;Acknowledgments;509
14.4.7;References;509
14.5;Chapter 32. The eighteenth C.U. Ariëns Kappers lecture: an introduction;514
14.5.1;C.U. Ariëns Kappers and the Central Institute for Brain Research in Amsterdam;514
14.6;Chapter 33. Molecular control of brain plasticity and repair;518
14.6.1;Mechanisms of recovery after CNS damage;518
14.6.2;Plasticity in recovery of function;519
14.6.3;Plasticity decreases with age;519
14.6.4;Methods of restoring plasticity in the adult CNS;520
14.6.5;Chondroitinase and CSPGs;520
14.6.6;NogoA and plasticity;522
14.6.7;Inosine;522
14.6.8;Promoting plasticity opens a window of opportunity for rehabilitation;523
14.6.9;Do the treatments that restore plasticity also promote axon regenerationquest;524
14.6.10;How might therapies be combined to treat spinal cord injuryquest;524
14.6.11;References;524
15;Subject Index;528