Autophagy impairment in Parkinson's disease

被引:112
|
作者
Karabiyik, Cansu [1 ]
Lee, Min Jae [2 ]
Rubinsztein, David C. [1 ,3 ]
机构
[1] Cambridge Inst Med Res, Dept Med Genet, Cambridge Biomed Campus,Wellcome Trust MRC Bldg, Cambridge CB2 0XY, England
[2] Seoul Natl Univ, Coll Med, Dept Biochem & Mol Biol, Seoul 03080, South Korea
[3] UK Dementia Res Inst, Cambridge Biomed Campus,Hills Rd, Cambridge, England
来源
SIGNALLING MECHANISMS IN AUTOPHAGY | 2017年 / 61卷 / 06期
基金
英国惠康基金;
关键词
ALPHA-SYNUCLEIN DEGRADATION; LYSOSOMAL DYSFUNCTION; REGULATE AUTOPHAGY; DOPAMINE NEURONS; MUTATIONS; COMPLEX; PINK1; NEURODEGENERATION; TRAFFICKING; DROSOPHILA;
D O I
10.1042/EBC20170023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Parkinson's disease (PD) is a debilitating movement disorder typically associated with the accumulation of intracytoplasmic aggregate prone protein deposits. Over recent years, increasing evidence has led to the suggestion that the mutations underlying certain forms of PD impair autophagy. Autophagy is a degradative pathway that delivers cytoplasmic content to lysosomes for degradation and represents a major route for degradation of aggregated cellular proteins and dysfunctional organelles. Autophagy up-regulation is a promising therapeutic strategy that is being explored for its potential to protect cells against the toxicity of aggregate-prone proteins in neurodegenerative diseases. Here, we describe how the mutations in different subtypes of PD can affect different stages of autophagy.
引用
收藏
页码:711 / 720
页数:10
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