Molecular pathophysiology of Parkinson's disease

被引:975
作者
Moore, DJ [1 ]
West, AB
Dawson, VL
Dawson, TM
机构
[1] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA
关键词
alpha-synuclein; parkin; mitochondrial complex-I; ubiquitin-proteasome system; oxidative stress;
D O I
10.1146/annurev.neuro.28.061604.135718
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Although the etiology of PD is incompletely understood, the recent discovery of genes associated with rare monogenic forms of the disease, together with earlier studies and new experimental animal models, has provided important and novel insight into the molecular pathways involved in disease pathogenesis. Increasing evidence indicates that deficits in mitochondrial function, oxidative and nitrosative stress, the accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways or events that commonly underlie the pathogenesis of sporadic and familial forms of PD.
引用
收藏
页码:57 / 87
页数:31
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