Mitochondria as a therapeutic target in Alzheimer's disease

被引:29
|
作者
Wang, Jian [1 ]
Chen, Guo-Jun [1 ]
机构
[1] Chongqing Med Univ, Chongqing Key Lab Neurol, Affiliated Hosp 1, Dept Neurol, 1 Youyi Rd, Chongqing 400016, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; Antioxidant; Biogenesis; Dynamics; Mitochondria; mtDNA; Therapy;
D O I
10.1016/j.gendis.2016.05.001
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) remains the most common neurodegenerative disease characterized by beta-amyloid protein (A beta) deposition and memory loss. Studies have shown that mitochondrial dysfunction plays a crucial role in AD, which involves oxidative stress-induced respiratory chain dysfunction, loss of mitochondrial biogenesis, defects of mitochondrial dynamics and mtDNA mutations. Thus mitochondria might serve as drug therapy target for AD. In this article, we first briefly discussed mitochondrial theory in the development of AD, and then we summarized recent advances of mitochondrial abnormalities in AD pathology and introduced a series of drugs and techniques targeting mitochondria. We think that maintaining mitochondrial function may provide a new way of thinking in the treatment of AD. Copyright (C) 2016, Chongqing Medical University. Production and hosting by Elsevier B.V.
引用
收藏
页码:220 / 227
页数:8
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