Molecular Dysfunctions of Mitochondria-Associated Membranes (MAMs) in Alzheimer's Disease

被引:47
作者
Eysert, Fanny [1 ]
Kinoshita, Paula Fernanda [1 ,2 ]
Mary, Arnaud [1 ]
Vaillant-Beuchot, Loan [1 ]
Checler, Frederic [1 ]
Chami, Mounia [1 ]
机构
[1] Univ Cote dAzur, CNRS, INSERM, Lab Excellence DistAlz,Inst Mol & Cellular Pharma, F-06560 Valbonne, France
[2] Univ Sao Paulo, Dept Pharmacol, Inst Ciencias Biomed, BR-05508900 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
endoplasmic reticulum (ER); mitochondria; mitochondria-associated membranes (MAMs); Alzheimer’ s disease (AD); calcium signaling; phospholipids; cholesterol; fatty acid; lipids; unfolded protein response (UPR); APOE; tau; β amyloid precursor protein (APP); amyloid β peptide (Aβ APP-C-terminal fragments (APP-CTFs); UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS; AMYLOID PRECURSOR PROTEIN; C-TERMINAL FRAGMENT; APOLIPOPROTEIN-E; MOUSE MODEL; BETA-SECRETASE; A-BETA; GAMMA-SECRETASE; ABNORMAL INTERACTION;
D O I
10.3390/ijms21249521
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 a multifactorial neurodegenerative pathology characterized by a progressive decline of cognitive functions. Alteration of various signaling cascades affecting distinct subcellular compartment functions and their communication likely contribute to AD progression. Among others, the alteration of the physical association between the endoplasmic reticulum (ER) and mitochondria, also referred as mitochondria-associated membranes (MAMs), impacts various cellular housekeeping functions such as phospholipids-, glucose-, cholesterol-, and fatty-acid-metabolism, as well as calcium signaling, which are all altered in AD. Our review describes the physical and functional proteome crosstalk between the ER and mitochondria and highlights the contribution of distinct molecular components of MAMs to mitochondrial and ER dysfunctions in AD progression. We also discuss potential strategies targeting MAMs to improve mitochondria and ER functions in AD.
引用
收藏
页码:1 / 29
页数:28
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