Abstract
Parkinsons disease (PD) is characterized clinically by resting tremor, rigidity, bradykinesia and postural instability due to progressive and selective loss of dopamine neurons in the ventral substantia nigra, with the presence of ubiquitinated protein deposits called Lewy bodies in the neurons. The pathoetiology of cell death in PD is incompletely understood and evidence implicates impaired mitochondrial complex I function, altered intracellular redox state, activation of proapoptotic factors and dysfunction of ubiquitinproteasome pathway. Now it is believed that genetic aberration, an environmental toxin or combination of both leads to a cascade of events culminating in the destruction of myelinated brainstem catecholaminergic neurons. Also the role of production of significant levels of abnormal proteins, which may misfold, aggregate and interfere with intracellular processes causing cytotoxicity has recently been hypothesized. In this article, the diverse pieces of evidence that have linked the various factors responsible for the pathophysiology of PD are reviewed with special emphasis to various candidate genes and proteins. Furthermore, the present therapeutic strategies and futuristic approaches for the pharmacotherapy of PD are critically discussed.
Keywords: Parkinson's disease., lewy bodies, protein aggregation, pathophysiology, α-Synuclein, Parkin, Mitochondrial dysfunction
Current Neuropharmacology
Title: Parkinsons Disease: Genetics and Beyond
Volume: 5 Issue: 2
Author(s): N. N. Inamdar, D. K. Arulmozhi, A. Tandon and S. L. Bodhankar
Affiliation:
Keywords: Parkinson's disease., lewy bodies, protein aggregation, pathophysiology, α-Synuclein, Parkin, Mitochondrial dysfunction
Abstract: Parkinsons disease (PD) is characterized clinically by resting tremor, rigidity, bradykinesia and postural instability due to progressive and selective loss of dopamine neurons in the ventral substantia nigra, with the presence of ubiquitinated protein deposits called Lewy bodies in the neurons. The pathoetiology of cell death in PD is incompletely understood and evidence implicates impaired mitochondrial complex I function, altered intracellular redox state, activation of proapoptotic factors and dysfunction of ubiquitinproteasome pathway. Now it is believed that genetic aberration, an environmental toxin or combination of both leads to a cascade of events culminating in the destruction of myelinated brainstem catecholaminergic neurons. Also the role of production of significant levels of abnormal proteins, which may misfold, aggregate and interfere with intracellular processes causing cytotoxicity has recently been hypothesized. In this article, the diverse pieces of evidence that have linked the various factors responsible for the pathophysiology of PD are reviewed with special emphasis to various candidate genes and proteins. Furthermore, the present therapeutic strategies and futuristic approaches for the pharmacotherapy of PD are critically discussed.
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Cite this article as:
Inamdar N. N., Arulmozhi K. D., Tandon A. and Bodhankar L. S., Parkinsons Disease: Genetics and Beyond, Current Neuropharmacology 2007; 5 (2) . https://dx.doi.org/10.2174/157015907780866893
DOI https://dx.doi.org/10.2174/157015907780866893 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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