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帕金森病中的自噬缺陷:遗传学的启示。

Defective autophagy in Parkinson's disease: lessons from genetics.

机构信息

Center of Parkinson's Disease Beijing Institute for Brain Disorders, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Department of Neurobiology Capital Medical University, Beijing, 100069, China.

出版信息

Mol Neurobiol. 2015 Feb;51(1):89-104. doi: 10.1007/s12035-014-8787-5. Epub 2014 Jul 4.

Abstract

Parkinson's disease (PD) is the most prevalent neurodegenerative movement disorder. Genetic studies over the past two decades have greatly advanced our understanding of the etiological basis of PD and elucidated pathways leading to neuronal degeneration. Recent studies have suggested that abnormal autophagy, a well conserved homeostatic process for protein and organelle turnover, may contribute to neurodegeneration in PD. Moreover, many of the proteins related to both autosomal dominant and autosomal recessive PD, such as α-synuclein, PINK1, Parkin, LRRK2, DJ-1, GBA, and ATPA13A2, are also involved in the regulation of autophagy. We propose that reduced autophagy enhances the accumulation of α-synuclein, other pathogenic proteins, and dysfunctional mitochondria in PD, leading to oxidative stress and neuronal death.

摘要

帕金森病(PD)是最常见的神经退行性运动障碍。过去二十年的遗传研究极大地促进了我们对 PD 的病因基础的理解,并阐明了导致神经元变性的途径。最近的研究表明,异常的自噬——一种用于蛋白质和细胞器更新的高度保守的动态平衡过程——可能导致 PD 的神经退行性变。此外,许多与常染色体显性和常染色体隐性 PD 相关的蛋白质,如α-突触核蛋白、PINK1、Parkin、LRRK2、DJ-1、GBA 和 ATPA13A2,也参与自噬的调节。我们提出,自噬减少会增强 PD 中α-突触核蛋白、其他致病蛋白和功能失调线粒体的积累,导致氧化应激和神经元死亡。

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