Neurodegeneration and Neuroprotection in Parkinson Disease

被引:151
|
作者
Fahn S. [1 ]
Sulzer D. [1 ]
机构
[1] Department of Neurology, Columbia University, New York
来源
NeuroRX | 2004年 / 1卷 / 1期
关键词
alpha-synuclein; PARK genes; Parkin gene; ubiquitin pathway;
D O I
10.1602/neurorx.1.1.139
中图分类号
学科分类号
摘要
Many of the motoric features that define Parkinson disease (PD) result primarily from the loss of the neuromelanin (NM)-containing dopamine (DA) neurons of the substantia nigra (SN), and to a lesser extent, other mostly catecholaminergic neurons, and are associated with cytoplasmic "Lewy body" inclusions in some of the surviving neurons. While there are uncommon instances of familial PD, and rare instances of known genetic causes, the etiology of the vast majority of PD cases remains unknown (i.e., idiopathic). Here we outline genetic and environmental findings related to PD epidemiology, suggestions that aberrant protein degradation may play a role in disease pathogenesis, and pathogenetic mechanisms including oxidative stress due to DA oxidation that could underlie the selectivity of neurodegeneration. We then outline potential approaches to neuroprotection for PD that are derived from current notions on disease pathogenesis. © 2004 The American Society for Experimental NeuroTherapeutics, Inc.
引用
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页码:139 / 154
页数:15
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