Autophagy deregulation in neurodegenerative diseases - recent advances and future perspectives

被引:102
作者
Cheung, Zelda H.
Ip, Nancy Y. [1 ]
机构
[1] Hong Kong Univ Sci & Technol, Div Life Sci, Mol Neurosci Ctr, Kowloon, Hong Kong, Peoples R China
关键词
Alzheimer's disease; Huntington's disease; macroautophagy; mitophagy; Parkinson's disease; ALPHA-SYNUCLEIN; MUTANT HUNTINGTIN; CELL-DEATH; AMYLOID-BETA; MEDIATED AUTOPHAGY; BASAL AUTOPHAGY; PARKINSONS; DEGRADATION; TOXICITY; MODELS;
D O I
10.1111/j.1471-4159.2011.07314.x
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
Autophagy is an evolutionarily conserved homeostatic process for the turnover of cellular contents, organelles and misfolded proteins through the lysosomal machinery. Recently, the involvement of autophagy in the pathophysiology of neurodegenerative diseases has attracted considerable interest because autophagy deregulation has been linked to some of these neurodegenerative disorders. This interest is further heightened by the demonstration that various autophagic pathways, including macroautophagy and chaperone-mediated autophagy, are implicated in the turnover of proteins that are prone to aggregation in cellular or animal disease models. These observations have stimulated new awareness in the pivotal role of the autophagic pathways in neurodegenerative disease pathophysiology, and have sparked extensive research aimed at deciphering the mechanisms by which autophagy is altered in these disorders. Here, we summarize the latest advances in our understanding of the role of autophagy deregulation in Parkinson's, Alzheimer's and Huntington's disease.
引用
收藏
页码:317 / 325
页数:9
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