Published since 1959, International Review of Neurobiology is a well-known series appealing to neuroscientists, clinicians, psychologists, physiologists, and pharmacologists. Led by an internationally renowned editorial board, this important serial publishes both eclectic volumes made up of timely reviews and thematic volumes that focus on recent progress in a specific area of neurobiology research.
With recent advancements in new knowledge, it has become evident that psychostimulants and related drugs of abuse are influencing our central nervous system (CNS) remarkably and could alter their function for a longtime. This volume is the first to focus on substance abuse induced brain pathology in the widest sense as it covers alterations in neuronal, glial and endothelial cell functions under the influence of acute or chronic usage of substance abuse.
1. Introduction 2. Cell therapy for Parkinson's disease 3. Midbrain dopamine neurons 4. Isolation of transplantable midbrain dopamine neurons from stem cell-derived populations 5. Reporter mice as tools in neural transplantation studies 6. Isolation of midbrain dopamine neuronal precursors from the developing midbrain 7. Graft composition and its relevance for functional impact 8. Reconstruction of the nigro-striatal pathway through intra-nigral grafting 9. Concluding remarks 10. Developing novel immunogens for a safe and effective Alzheimer's disease vaccine 11. Introduction 12. Aβ immunotherapy in rodents, monkeys, and humans 13. Novel short Aβ immunogens for active vaccination 14. Conclusions 15. Acknowedgments 16. Innate immunity in the nervous system 17. The complement system 18. Activation and regulation of the complement system 19. The role of complement in inflammation 20. Complement in the central nervous system (CNS) 21. Complement in the peripheral nervous system (PNS) 22. Complement regulation in nerve injury and disease: a therapeutic approach 23. Abbreviations 24. Acknowledgment 25. Neuroinflammation in spinal cord injury: therapeutic targets for neuroprotection and regeneration 26. Introduction to spinal cord injury (SCI) pathology: neuroinflammation in the pathogenesis of secondary injury 27. Manipulating neuroinflammation to improve recovery from SCI 28. Consequences of neuroinflammation on neuronal plasticity and regeneration 29. Conclusions 30. Acknowledgments 31. Toll-like receptors in the CNS: implications for neurodegeneration and repair 32. Introduction and scope of this chapter 33. General features of TLRs 34. Expression and function of TLRs in microglia 35. Expression and function of TLRs in astrocytes 36. Expression and function of TLRs in neurons 37. Concluding remarks and future perspectives 38. Abbreviations 39. Acknowledgements 40. Gene therapy and transplantation in the retinofugal pathway 41. Introduction 42. AAV-mediated transduction of retinal ganglion cells 43. Use of LV to genetically modify Schwann cells in chimeric peripheral nerve grafts 44. Transduction and tropic properties of modified AAV vectors in the retina 45. Dendritic morphology of RGCs transduced with AAV encoding different genes 46. Concluding comments 47. Controlled dissemination of AAV vectors in the primate brain 48. Introduction 49. Trafficking of AAV in the brain 50. Real-time imaging 51. Clinical implications 52. Conclusion 53. From microsurgery to nanosurgery: how viral vectors may help repair the peripheral nerve 54. Introduction: peripheral nerve repair 55. Molecular mechanisms involved in peripheral nerve regeneration 56. Current challenges in peripheral nerve repair 57. Viral vectors: promising tools to express potentially therapeutic proteins in injured peripheral nerves 58. Lentiviral vector-mediated overexpression of neurotrophic factors to enhance nerve regeneration 59. Exogenous neurotrophic factors: precise time- and location-specific application is necessary to promote outgrowth 60. Enhancing motoneuron survival as an application of neurotrophic factors 61. Failed functional recovery: misrouting of regenerating axons is an important factor 62. Addressing the routing problem at a molecular level 63. Future perspective: the continuing miniaturization of surgical and diagnostic tools 64. Gene therapy for neurodegenerative diseases based on lentiviral vectors 65. Lentiviral vector-mediated gene therapy 66. Amyotrophic lateral sclerosis 67. Spinal muscular atrophy 68. Parkinson's disease 69. Huntington's disease 70. Clinical prospects and challenges of lentiviral vectors 71. Abbreviations 72. Trophic factors therapy in Parkinson's disease 73. Parkinson's disease and neurotrophic factors 74. Glial cell line-derived neurotrophic factor 75. Neurturin 76. Conclusion 77. Progesterone as a neuroprotective factor in traumatic and ischemic brain injury 78. Introduction 79. Neuroprotective effects of progesterone in TBI 80. Stroke and progesterone 81. Progesterone's neuroprotective mechanisms 82. Conclusion 83. Abbreviations 84. Acknowledgment 85. Estrogen and testosterone therapies in multiple sclerosis 86. Introduction 87. Potential mechanisms of sex hormones 88. Sex hormone treatments in MS 89. Conclusions and future directions 90. Abbreviations 91. Acknowledgments 92. Treatment of retinal diseases with VEGF antagonists 93. Introduction 94. Ocular angiogenesis 95. Mechanisms of angiogenesis and wound healing 96. Role of VEGF in ocular pathology and clinical use of VEGF antagonists 97. VEGF antagonists in conditions with preretinal neovascularization 98. VEGF antagonists in AMD and other conditions with subretinal neovascularization 99. Side effects of ocular use of VEGF antagonists 100. Conclusion 101. Pharmacological modification of the extracellular matrix to promote regeneration of the injured brain and spinal cord 102. Introduction 103. Lesion scarring after CNS injury 104. Differences in axonal growth responses to scar formation 105. Therapies to prevent fibrous scar formation 106. Pharmacological inhibition of scarring with iron chelators 107. Conclusion 108. Abbreviations 109. Acknowledgments 110. The placebo response: neurobiological and clinical issues of neurological relevance 111. Introduction 112. Two different meanings of the term “placebo effect” 113. Evolution of the sugar pill 114. The placebo response: reflex or cognitive? 115. Neurological disorders showing prominent placebo effects 116. From research to clinical practice 117. Conclusions 118. Acknowledgment 119. Brain–computer interfaces: an overview of the hardware to record neural signals from the cortex 120. Introduction to neuroprostheses 121. Classification of BCI 122. Extracorporeal electrodes for class I BCI 123. Epicortical electrodes for class II BCI 124. Intracortical electrodes for class III BCI 125. Comparison of BCI approaches 126. Concluding remarks 127. Acknowledgments 128. Artificial vision: needs, functioning, and testing of a retinal electronic prosthesis 129. Retinal degenerative diseases: an overview 130. Prospects for therapies available to RD patients 131. Electron prosthetic devices: general considerations 132. Morphological and neuronal bases for implantation of a retinal prosthesis 133. Central connections in retinal degeneration and prosthesis implantation 134. Visual perception: measurements in low vision and brain processing after therapeutic intervention 135. A clinical trial and testing of an epiretinal prosthetic device 136. Future studies 137. Progress in restoration of hearing with the auditory brainstem implant 138. Introduction 139. Cochlear implants 140. Brainstem implants 141. Conclusions 142. Microstimulation of visual cortex to restore vision 143. Introduction 144. Microstimulation of V1 elicits saccadic eye movements 145. Microstimulation of V1 delays the execution of visually guided saccades 146. Microstimulation of V1 elicits a detection response 147. Can microstimulation of V1 evoke phosphenes exhibiting features? 148. Effects of blindness on phosphene induction 149. Discussion 150. Conclusions 151. Abbreviations 152. Acknowledgment 153. Functional neurosurgery for movement disorders: a historical perspective 154. Introduction 155. Therapy for movement disorders: a random walk around a logical thread 156. What is the current status of the efficiency of high-frequency stimulation in various nuclei in different diseases? 157. Deep brain stimulation: a preferred tool in functional neurosurgery? 158. What did we learn from the practice of deep brain stimulation in human patients? 159. Conclusions 160. Recovery of control of posture and locomotion after a spinal cord injury: solutions staring us in the face 161. Why does spinal cord injury result in a loss of movement control? 162. Initiating, sustaining, and stopping movements: sources of control 163. Treatment paradigms for preserving muscle function after a spinal cord injury 164. Significance of the concept of “physiological state” of the spinal circuitry in relearning to step 165. Treatment paradigms for restoring locomotor control after a spinal cord injury 166. Integrating neuroengineering and biological concepts to regain posture and locomotion 167. Acknowledgments 168. Deep brain stimulation in obsessive–compulsive disorder 169. Introduction 170. DBS technique 171. Mechanism of action of DBS 172. Psychiatric comorbidity in DBS of neurological disorders 173. Obsessive–compulsive disorder 174. Clinical efficacy of DBS in OCD 175. Side effects of DBS in OCD 176. Conclusion and future 177. The use of repetitive transcranial magnetic stimulation (rTMS) for the treatment of spasticity 178. Introduction 179. Pathophysiology of spasticity 180. Effects of rTMS on cortical excitability 181. Effects of rTMS on spinal excitability 182. Effects of rTMS in patients with spasticity 183. Conclusions 184. Abbreviations 185. Calcium signaling and the development of specific neuronal connections 186. Introduction 187. Axonal growth cone navigation 188. Synaptic partner selection by dendritic filopodia 189. Refinement of synaptic connections 190. Conclusion 191. Acknowledgments 192. Remyelination in multiple sclerosis 193. Introduction 194. Demyelinated MS lesions with persistence of cells of the oligodendrocyte lineage 195. Lesions with oligodendroglial depopulation 196. Conclusion 197. Acknowledgments 198. Magnetic resonance techniques to quantify tissue damage, tissue repair, and functional cortical reorganization in multiple sclerosis 199. Introduction 200. Imaging brain atrophy 201. Intrinsic lesion damage 202. Imaging “diffuse” normal-appearing brain tissue (NABT) and normal-appearing WM (NAWM) damage 203. Imaging “diffuse” GM damage 204. Cortical reorganization 205. Imaging the spinal cord 206. Imaging the optic nerve 207. Conclusions 208. MRI of neuronal network structure, function, and plasticity 209. Introduction 210. Diffusion tensor imaging 211. Resting state fMRI 212. Discussion 213. Abbreviations 214. Acknowledgments 215. The eighteenth C.U. Ariëns Kappers lecture: an introduction 216. C.U. Ariëns Kappers and the Central Institute for Brain Research in Amsterdam 217. Molecular control of brain plasticity and repair 218. Mechanisms of recovery after CNS damage 219. Plasticity in recovery of function 220. Plasticity decreases with age 221. Methods of restoring plasticity in the adult CNS 222. Chondroitinase and CSPGs 223. NogoA and plasticity 224. Inosine 225. Promoting plasticity opens a window of opportunity for rehabilitation 226. Do the treatments that restore plasticity also promote axon regeneration? 227. How might therapies be combined to treat spinal cord injury?
Published since 1959, International Review of Neurobiology is a well-known series appealing to neuroscientists, clinicians, psychologists, physiologists, and pharmacologists. Led by an internationally renowned editorial board, this important serial publishes both eclectic volumes made up of timely reviews and thematic volumes that focus on recent progress in a specific area of neurobiology research.
With recent advancements in new knowledge, it has become evident that psychostimulants and related drugs of abuse are influencing our central nervous system (CNS) remarkably and could alter their function for a longtime. This volume is the first to focus on substance abuse induced brain pathology in the widest sense as it covers alterations in neuronal, glial and endothelial cell functions under the influence of acute or chronic usage of substance abuse.
1. Introduction 2. Cell therapy for Parkinson's disease 3. Midbrain dopamine neurons 4. Isolation of transplantable midbrain dopamine neurons from stem cell-derived populations 5. Reporter mice as tools in neural transplantation studies 6. Isolation of midbrain dopamine neuronal precursors from the developing midbrain 7. Graft composition and its relevance for functional impact 8. Reconstruction of the nigro-striatal pathway through intra-nigral grafting 9. Concluding remarks 10. Developing novel immunogens for a safe and effective Alzheimer's disease vaccine 11. Introduction 12. Aβ immunotherapy in rodents, monkeys, and humans 13. Novel short Aβ immunogens for active vaccination 14. Conclusions 15. Acknowedgments 16. Innate immunity in the nervous system 17. The complement system 18. Activation and regulation of the complement system 19. The role of complement in inflammation 20. Complement in the central nervous system (CNS) 21. Complement in the peripheral nervous system (PNS) 22. Complement regulation in nerve injury and disease: a therapeutic approach 23. Abbreviations 24. Acknowledgment 25. Neuroinflammation in spinal cord injury: therapeutic targets for neuroprotection and regeneration 26. Introduction to spinal cord injury (SCI) pathology: neuroinflammation in the pathogenesis of secondary injury 27. Manipulating neuroinflammation to improve recovery from SCI 28. Consequences of neuroinflammation on neuronal plasticity and regeneration 29. Conclusions 30. Acknowledgments 31. Toll-like receptors in the CNS: implications for neurodegeneration and repair 32. Introduction and scope of this chapter 33. General features of TLRs 34. Expression and function of TLRs in microglia 35. Expression and function of TLRs in astrocytes 36. Expression and function of TLRs in neurons 37. Concluding remarks and future perspectives 38. Abbreviations 39. Acknowledgements 40. Gene therapy and transplantation in the retinofugal pathway 41. Introduction 42. AAV-mediated transduction of retinal ganglion cells 43. Use of LV to genetically modify Schwann cells in chimeric peripheral nerve grafts 44. Transduction and tropic properties of modified AAV vectors in the retina 45. Dendritic morphology of RGCs transduced with AAV encoding different genes 46. Concluding comments 47. Controlled dissemination of AAV vectors in the primate brain 48. Introduction 49. Trafficking of AAV in the brain 50. Real-time imaging 51. Clinical implications 52. Conclusion 53. From microsurgery to nanosurgery: how viral vectors may help repair the peripheral nerve 54. Introduction: peripheral nerve repair 55. Molecular mechanisms involved in peripheral nerve regeneration 56. Current challenges in peripheral nerve repair 57. Viral vectors: promising tools to express potentially therapeutic proteins in injured peripheral nerves 58. Lentiviral vector-mediated overexpression of neurotrophic factors to enhance nerve regeneration 59. Exogenous neurotrophic factors: precise time- and location-specific application is necessary to promote outgrowth 60. Enhancing motoneuron survival as an application of neurotrophic factors 61. Failed functional recovery: misrouting of regenerating axons is an important factor 62. Addressing the routing problem at a molecular level 63. Future perspective: the continuing miniaturization of surgical and diagnostic tools 64. Gene therapy for neurodegenerative diseases based on lentiviral vectors 65. Lentiviral vector-mediated gene therapy 66. Amyotrophic lateral sclerosis 67. Spinal muscular atrophy 68. Parkinson's disease 69. Huntington's disease 70. Clinical prospects and challenges of lentiviral vectors 71. Abbreviations 72. Trophic factors therapy in Parkinson's disease 73. Parkinson's disease and neurotrophic factors 74. Glial cell line-derived neurotrophic factor 75. Neurturin 76. Conclusion 77. Progesterone as a neuroprotective factor in traumatic and ischemic brain injury 78. Introduction 79. Neuroprotective effects of progesterone in TBI 80. Stroke and progesterone 81. Progesterone's neuroprotective mechanisms 82. Conclusion 83. Abbreviations 84. Acknowledgment 85. Estrogen and testosterone therapies in multiple sclerosis 86. Introduction 87. Potential mechanisms of sex hormones 88. Sex hormone treatments in MS 89. Conclusions and future directions 90. Abbreviations 91. Acknowledgments 92. Treatment of retinal diseases with VEGF antagonists 93. Introduction 94. Ocular angiogenesis 95. Mechanisms of angiogenesis and wound healing 96. Role of VEGF in ocular pathology and clinical use of VEGF antagonists 97. VEGF antagonists in conditions with preretinal neovascularization 98. VEGF antagonists in AMD and other conditions with subretinal neovascularization 99. Side effects of ocular use of VEGF antagonists 100. Conclusion 101. Pharmacological modification of the extracellular matrix to promote regeneration of the injured brain and spinal cord 102. Introduction 103. Lesion scarring after CNS injury 104. Differences in axonal growth responses to scar formation 105. Therapies to prevent fibrous scar formation 106. Pharmacological inhibition of scarring with iron chelators 107. Conclusion 108. Abbreviations 109. Acknowledgments 110. The placebo response: neurobiological and clinical issues of neurological relevance 111. Introduction 112. Two different meanings of the term “placebo effect” 113. Evolution of the sugar pill 114. The placebo response: reflex or cognitive? 115. Neurological disorders showing prominent placebo effects 116. From research to clinical practice 117. Conclusions 118. Acknowledgment 119. Brain–computer interfaces: an overview of the hardware to record neural signals from the cortex 120. Introduction to neuroprostheses 121. Classification of BCI 122. Extracorporeal electrodes for class I BCI 123. Epicortical electrodes for class II BCI 124. Intracortical electrodes for class III BCI 125. Comparison of BCI approaches 126. Concluding remarks 127. Acknowledgments 128. Artificial vision: needs, functioning, and testing of a retinal electronic prosthesis 129. Retinal degenerative diseases: an overview 130. Prospects for therapies available to RD patients 131. Electron prosthetic devices: general considerations 132. Morphological and neuronal bases for implantation of a retinal prosthesis 133. Central connections in retinal degeneration and prosthesis implantation 134. Visual perception: measurements in low vision and brain processing after therapeutic intervention 135. A clinical trial and testing of an epiretinal prosthetic device 136. Future studies 137. Progress in restoration of hearing with the auditory brainstem implant 138. Introduction 139. Cochlear implants 140. Brainstem implants 141. Conclusions 142. Microstimulation of visual cortex to restore vision 143. Introduction 144. Microstimulation of V1 elicits saccadic eye movements 145. Microstimulation of V1 delays the execution of visually guided saccades 146. Microstimulation of V1 elicits a detection response 147. Can microstimulation of V1 evoke phosphenes exhibiting features? 148. Effects of blindness on phosphene induction 149. Discussion 150. Conclusions 151. Abbreviations 152. Acknowledgment 153. Functional neurosurgery for movement disorders: a historical perspective 154. Introduction 155. Therapy for movement disorders: a random walk around a logical thread 156. What is the current status of the efficiency of high-frequency stimulation in various nuclei in different diseases? 157. Deep brain stimulation: a preferred tool in functional neurosurgery? 158. What did we learn from the practice of deep brain stimulation in human patients? 159. Conclusions 160. Recovery of control of posture and locomotion after a spinal cord injury: solutions staring us in the face 161. Why does spinal cord injury result in a loss of movement control? 162. Initiating, sustaining, and stopping movements: sources of control 163. Treatment paradigms for preserving muscle function after a spinal cord injury 164. Significance of the concept of “physiological state” of the spinal circuitry in relearning to step 165. Treatment paradigms for restoring locomotor control after a spinal cord injury 166. Integrating neuroengineering and biological concepts to regain posture and locomotion 167. Acknowledgments 168. Deep brain stimulation in obsessive–compulsive disorder 169. Introduction 170. DBS technique 171. Mechanism of action of DBS 172. Psychiatric comorbidity in DBS of neurological disorders 173. Obsessive–compulsive disorder 174. Clinical efficacy of DBS in OCD 175. Side effects of DBS in OCD 176. Conclusion and future 177. The use of repetitive transcranial magnetic stimulation (rTMS) for the treatment of spasticity 178. Introduction 179. Pathophysiology of spasticity 180. Effects of rTMS on cortical excitability 181. Effects of rTMS on spinal excitability 182. Effects of rTMS in patients with spasticity 183. Conclusions 184. Abbreviations 185. Calcium signaling and the development of specific neuronal connections 186. Introduction 187. Axonal growth cone navigation 188. Synaptic partner selection by dendritic filopodia 189. Refinement of synaptic connections 190. Conclusion 191. Acknowledgments 192. Remyelination in multiple sclerosis 193. Introduction 194. Demyelinated MS lesions with persistence of cells of the oligodendrocyte lineage 195. Lesions with oligodendroglial depopulation 196. Conclusion 197. Acknowledgments 198. Magnetic resonance techniques to quantify tissue damage, tissue repair, and functional cortical reorganization in multiple sclerosis 199. Introduction 200. Imaging brain atrophy 201. Intrinsic lesion damage 202. Imaging “diffuse” normal-appearing brain tissue (NABT) and normal-appearing WM (NAWM) damage 203. Imaging “diffuse” GM damage 204. Cortical reorganization 205. Imaging the spinal cord 206. Imaging the optic nerve 207. Conclusions 208. MRI of neuronal network structure, function, and plasticity 209. Introduction 210. Diffusion tensor imaging 211. Resting state fMRI 212. Discussion 213. Abbreviations 214. Acknowledgments 215. The eighteenth C.U. Ariëns Kappers lecture: an introduction 216. C.U. Ariëns Kappers and the Central Institute for Brain Research in Amsterdam 217. Molecular control of brain plasticity and repair 218. Mechanisms of recovery after CNS damage 219. Plasticity in recovery of function 220. Plasticity decreases with age 221. Methods of restoring plasticity in the adult CNS 222. Chondroitinase and CSPGs 223. NogoA and plasticity 224. Inosine 225. Promoting plasticity opens a window of opportunity for rehabilitation 226. Do the treatments that restore plasticity also promote axon regeneration? 227. How might therapies be combined to treat spinal cord injury?
