The contribution of mitochondria-associated endoplasmic reticulum membranes (MAMs) dysfunction in Alzheimer's disease and the potential countermeasure

被引:13
|
作者
Li, Zehui [1 ]
Cao, Yu [1 ]
Pei, Hui [1 ]
Ma, Lina [1 ]
Yang, Yang [1 ]
Li, Hao [1 ,2 ]
机构
[1] China Acad Chinese Med Sci, Xiyuan Hosp, Dept Geriatr, Beijing, Peoples R China
[2] China Acad Chinese Med Sci, Wangjing Hosp, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; mitochondria; endoplasmic reticulum; calcium homeostasis; lipid metabolism; AMYLOID-BETA; APP/PS1; MICE; PATHOGENESIS; CHOLESTEROL; PROTEIN; INVOLVEMENT; BRAIN; MODEL;
D O I
10.3389/fnins.2023.1158204
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) is the most common neurodegenerative disease. There are many studies targeting extracellular deposits of amyloid beta-peptide (A beta) and intracellular neurofibrillary tangles (NFTs), however, there are no effective treatments to halt the progression. Mitochondria-associated endoplasmic reticulum membranes (MAMs) have long been found to be associated with various pathogenesis hypotheses of AD, such as A beta deposition, mitochondrial dysfunction, and calcium homeostasis. However, there is a lack of literature summarizing recent advances in the mechanism and treatment studies. Accordingly, this article reviews the latest research involving the roles of MAM structure and tethering proteins in the pathogenesis of AD and summarizes potential strategies targeting MAMs to dissect treatment perspectives for AD.
引用
收藏
页数:7
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