Dysfunctional autophagy in Alzheimer's disease: pathogenic roles and therapeutic implications

被引:71
作者
Liang, Jun-Hua [1 ]
Jia, Jian-Ping [1 ]
机构
[1] Capital Med Univ, Xuan Wu Hosp, Dept Neurol, Beijing 100053, Peoples R China
关键词
Alzheimer's disease; autophagy; presenilin; axon; lysosome; animal model; AMYLOID-BETA; MOUSE MODEL; PROTEIN-DEGRADATION; NEURONAL AUTOPHAGY; UBIQUITIN; SYSTEM; INJURY; NEURODEGENERATION; MACROAUTOPHAGY; PROTEOLYSIS;
D O I
10.1007/s12264-013-1418-8
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer's disease (AD). The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.
引用
收藏
页码:308 / 316
页数:9
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