α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies

被引:667
作者
Wong, Yvette C. [1 ]
Krainc, Dimitri [1 ]
机构
[1] Northwestern Univ, Dept Neurol, Feinberg Sch Med, Chicago, IL 60611 USA
关键词
MULTIPLE-SYSTEM ATROPHY; A-BETA COMPONENT; CHAPERONE-MEDIATED AUTOPHAGY; SPORADIC PARKINSONS-DISEASE; MIDBRAIN DOPAMINE NEURONS; SUBSTANTIA-NIGRA NEURONS; TRANSGENIC MOUSE MODEL; LEWY BODY; IN-VIVO; ALZHEIMERS-DISEASE;
D O I
10.1038/nm.4269
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
Alterations in a-synuclein dosage lead to familial Parkinson's disease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Furthermore, alpha-synuclein contributes to the fibrilization of amyloid-beta and tau, two key proteins in Alzheimer's disease, which suggests a central role for alpha-synuclein toxicity in neurodegeneration. Recent studies of factors contributing to alpha-synuclein toxicity and its disruption of downstream cellular pathways, have expanded our understanding of disease pathogenesis in synucleinopathies.
引用
收藏
页码:151 / 163
页数:13
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