Expanding insights of mitochondrial dysfunction in Parkinson's disease

被引：719

作者：

Abou-Sleiman, PM ^{[1
]}

Muqit, MMK ^{[1
]}

Wood, NW ^{[1
]}

机构：

[1] Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England

来源：

NATURE REVIEWS NEUROSCIENCE | 2006年 / 7卷 / 03期

关键词：

D O I：

10.1038/nrn1868

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

The quest to disentangle the aetiopathogenesis of Parkinson's disease has been heavily influenced by the genes associated with the disease. The alpha-synuclein-centric theory of protein aggregation with the adjunct of parkin-driven proteasome deregulation has, in recent years, been complemented by the discovery and increasing knowledge of the functions of DJ1, PINK1 and OMI/HTRA2, which are all associated with the mitochondria and have been implicated in cellular protection against oxidative damage. We critically review how these genes fit into and enhance our understanding of the role of mitochondrial dysfunction in Parkinson's disease, and consider how oxidative stress might be a potential unifying factor in the aetiopathogenesis of the disease.

引用

页码：207 / 219

页数：13

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