- Title Pages
- Dedication
- Contributors
- Abbreviations
- 1 Death and survival in the nervous system
- 2 Axotomy and mechanical damage
- 3 Metabolic damage
- 4 Inflammation and demyelination
- 5 Infection
- 6 Neurodegenerative disease
- 7 Neuroprotection
- 8 Steroids
- 9 Trophic factors
- 10 Control of inflammation
- 11 Peripheral nerve regeneration
- 12 Failure of CNS regeneration
- 13 Anatomical plasticity
- 14 Biochemical plasticity
- 15 Remyelination
- 16 Coma
- 17 Motor, sensory, and autonomic function
- 18 Cognition
- 19 Psychiatric assessment
- 20 Pharmacological management
- 21 Neuropsychological rehabilitation
- 22 Axon regeneration in the CNS
- 23 Primary neuronal transplantation
- 24 Glial transplantation
- 25 Stem cells
- 26 Gene therapy
- Appendix 1 Alzheimer's disease
- Appendix 2 Amyotrophic lateral sclerosis (ALS)/Motor neurone disease
- Appendix 3 Creutzfeldt-Jakob disease (CJD)
- Appendix 4 Epilepsy
- Appendix 5 Huntington's disease
- Appendix 6 Multiple sclerosis
- Appendix 7 Parkinson's disease
- Appendix 8 Spinal-cord injury
- Appendix 9 Stroke
- References
- Index
Primary neuronal transplantation
Primary neuronal transplantation
- Chapter:
- (p.313) 23 Primary neuronal transplantation
- Source:
- Brain Damage, Brain Repair
- Author(s):
James W. Fawcett
Anne E. Rosser
Stephen B. Dunnett
- Publisher:
- Oxford University Press
Even though in a few situations we can now induce the damaged brain to repair itself by spontaneous reorganization and regeneration, there still remain many circumstances where intrinsic repair processes are ineffective. The most obvious situation is where there is progressive or complete loss of some one or other essential population of neurones that cannot be substituted by another (spared) set of neurones. For example, it has been observed that dopamine neurons have a remarkable capacity to undergo biochemical plasticity. Following partial damage of some neurones, the remaining dopamine neurones are upregulated and compensate for biochemical and functional loss. In Parkinson's disease, such plastic processes can retard the development of symptoms early in the disease, and pharmacological replacement strategies are clearly effective in the middle stages of the disease. However, as Parkinson's disease progresses, the drug response becomes dominated by devastating side-effects. It was in trying to resolve the issues of dopamine system repair that neuronal grafts were first found to be functionally effective. This problem guides the selection of examples and provides the main focus of discussion in this chapter.
Keywords: biochemical plasticity, neuronal transplantation, functional loss, replacement strategies, drug response, Parkinson's disease
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- Title Pages
- Dedication
- Contributors
- Abbreviations
- 1 Death and survival in the nervous system
- 2 Axotomy and mechanical damage
- 3 Metabolic damage
- 4 Inflammation and demyelination
- 5 Infection
- 6 Neurodegenerative disease
- 7 Neuroprotection
- 8 Steroids
- 9 Trophic factors
- 10 Control of inflammation
- 11 Peripheral nerve regeneration
- 12 Failure of CNS regeneration
- 13 Anatomical plasticity
- 14 Biochemical plasticity
- 15 Remyelination
- 16 Coma
- 17 Motor, sensory, and autonomic function
- 18 Cognition
- 19 Psychiatric assessment
- 20 Pharmacological management
- 21 Neuropsychological rehabilitation
- 22 Axon regeneration in the CNS
- 23 Primary neuronal transplantation
- 24 Glial transplantation
- 25 Stem cells
- 26 Gene therapy
- Appendix 1 Alzheimer's disease
- Appendix 2 Amyotrophic lateral sclerosis (ALS)/Motor neurone disease
- Appendix 3 Creutzfeldt-Jakob disease (CJD)
- Appendix 4 Epilepsy
- Appendix 5 Huntington's disease
- Appendix 6 Multiple sclerosis
- Appendix 7 Parkinson's disease
- Appendix 8 Spinal-cord injury
- Appendix 9 Stroke
- References
- Index