Autophagy in Parkinson's Disease

被引:14
|
作者
Nechushtai, Lior [1 ]
Frenkel, Dan [1 ]
Pinkas-Kramarski, Ronit [1 ]
机构
[1] Tel Aviv Univ, Sch Neurobiol Biochem & Biophys, Dept Neurobiol, IL-69978 Tel Aviv, Israel
关键词
apolipoprotein E4 (apoE4); autophagy; endocytosis; lysosomal degradation; Parkinson's disease (PD); synuclein alpha; ALPHA-SYNUCLEIN AGGREGATION; MITOCHONDRIAL DYSFUNCTION; APOLIPOPROTEIN-E; DOPAMINERGIC-NEURONS; IMPAIRS AUTOPHAGY; RISK; MECHANISMS; INHIBITION; DJ-1; GLUCOCEREBROSIDASE;
D O I
10.3390/biom13101435
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 devastating disease associated with accumulation of alpha-synuclein (alpha-Syn) within dopaminergic neurons, leading to neuronal death. PD is characterized by both motor and non-motor clinical symptoms. Several studies indicate that autophagy, an important intracellular degradation pathway, may be involved in different neurodegenerative diseases including PD. The autophagic process mediates the degradation of protein aggregates, damaged and unneeded proteins, and organelles, allowing their clearance, and thereby maintaining cell homeostasis. Impaired autophagy may cause the accumulation of abnormal proteins. Incomplete or impaired autophagy may explain the neurotoxic accumulation of protein aggregates in several neurodegenerative diseases including PD. Indeed, studies have suggested the contribution of impaired autophagy to alpha-Syn accumulation, the death of dopaminergic neurons, and neuroinflammation. In this review, we summarize the recent literature on the involvement of autophagy in PD pathogenesis.
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页数:16
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