AMPK: Potential Therapeutic Target for Alzheimer's Disease

被引:38
作者
Yang, Luping [1 ]
Jiang, Yijing [2 ,3 ]
Shi, Lihong [1 ]
Zhong, Dongling [1 ]
Li, Yuxi [1 ]
Li, Juan [1 ]
Jin, Rongjiang [1 ]
机构
[1] Chengdu Univ Tradit Chinese Med, Hlth Preservat & Rehabil Coll, Chengdu 610037, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Rehabil Hosp, Fuzhou 350003, Peoples R China
[3] Fujian Key Lab Rehabil Technol, Fuzhou 350003, Peoples R China
基金
中国国家自然科学基金;
关键词
AD; AMPK; A beta accumulation; tau phosphorylation; Alzheimer's disease; ACTIVATED PROTEIN-KINASE; ABNORMAL MITOCHONDRIAL DYNAMICS; AMYLOID-BETA; INSULIN-RESISTANCE; A-BETA; OXIDATIVE STRESS; SYNAPTIC DEGENERATION; STRUCTURAL BASIS; UPSTREAM KINASE; TAU-PROTEIN;
D O I
10.2174/1389203720666190819142746
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
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The pathogenesis of AD is very complicated. For decades, the amyloid hypothesis has influenced and guided research in the field of AD. Meanwhile, researchers gradually realized that AD is caused by multiple concomitant factors, such as autophagy, mitochondrial quality control, insulin resistance and oxidative stress. In current clinical trials, the improvement strategies of AD, such as A beta antibody immunotherapy and gamma secretase inhibitors, are limited. There is mounting evidence of neurodegenerative disorders indicated that activation of AMP-activated protein kinase (AMPK) may have broad neuroprotective effects. We reviewed the researches on AMPK for AD, the results demonstrated that activation of AMPK is controversial in A beta deposition and tau phosphorylation, but is positive to promote autophagy, maintain mitochondrial quality control, reduce insulin resistance and relieve oxidative stress. It is concluded that AMPK might be a new target for AD by aggressively treating the risk factors in the future.
引用
收藏
页码:66 / 77
页数:12
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