Parkinson's disease is the only neurodegenerative disorder for which the major pathological and biochemical defects have been identified. But why dopamine-containing cells in the substantia nigra die in Parkinson's disease remains a mystery. Similarly, the changes in basal ganglia output pathways which lead to the onset of motor disability and the occurrence of L-DOPA induced dyskinesia remain unclear. While treatment for the symptoms of Parkinson's disease is available, nothing can presently be done to stop the disease progressing.
A molecular approach to Parkinson's disease is unraveling genetic factors responsible for inducing the onset of nigral cell degeneration or for making individuals susceptible to other neurotoxic factors. Similarly, key findings in the area of mitochondrial dysfunction are now providing a new insight into the pathogenesis of Parkinson's disease. The application of molecular biochemistry to cell susceptibility and to the mechanisms of neuronal adapation occuring in basal ganglia are providing new clues to why motor abnormalities occur. Genetic engineering of cell lines, fibroblasts and viral vectors are providing means of replenishing dopamine production and introducing growth factors into the damaged basal ganglia. This book considers all these approaches and their implications for the future treatment of Parkinson's disease.
Proceedings of the Joint Conference of the 67th Annual Meeting of the German Association of Medical Informatics, Biometry, and Epidemiology e.V. (gmds) and the 14th Annual Meeting of the TMF
