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Mitochondria‐associated endoplasmic reticulum membranes: At the crossroad between familiar and sporadic Alzheimer's disease
Author(s) -
Wang Kangrun,
Zhang Wenling
Publication year - 2021
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.22196
Subject(s) - endoplasmic reticulum , autophagy , pathogenesis , mitochondrion , disease , alzheimer's disease , microbiology and biotechnology , dementia , hyperphosphorylation , biology , neuroscience , medicine , chemistry , pathology , biochemistry , apoptosis , phosphorylation
Alzheimer's disease (AD) is the leading cause of dementia and is incurable. The widely accepted amyloid hypothesis failed to produce efficient clinical therapies. In contrast, there is increasing evidence suggesting that the disruption of mitochondria‐associated endoplasmic reticulum (ER) membranes (MAM) is a critical upstream event of AD pathogenesis. Here, we review MAM's role in some AD symptoms such as plaque formation, tau hyperphosphorylation, synaptic loss, aberrant lipid synthesis, disturbed calcium homeostasis, and abnormal autophagy. At last, we proposed that MAM plays a central role in familial AD (FAD) and sporadic AD (SAD).