Critical review: involvement of endoplasmic reticulum stress in the aetiology of Alzheimer's disease

被引:116
作者
Hashimoto, Shoko [1 ]
Saido, Takaomi C. [1 ]
机构
[1] RIKEN, Ctr Brain Sci, Lab Proteolyt Neurosci, 2-1 Hirosawa, Wako, Saitama 3510198, Japan
来源
OPEN BIOLOGY | 2018年 / 8卷 / 04期
关键词
Alzheimer's disease; endoplasmic reticulum stress; unfolded protein response; App-knockin; APP/PS1; transgenic; UNFOLDED-PROTEIN RESPONSE; AMYLOID-BETA-PEPTIDE; INSULIN-DEGRADING ENZYME; LONG-TERM POTENTIATION; TAU-MEDIATED NEURODEGENERATION; OPERATED CALCIUM-ENTRY; INDUCED NEURONAL DEATH; BLOOD-BRAIN-BARRIER; ER STRESS; A-BETA;
D O I
10.1098/rsob.180024
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
The endoplasmic reticulum (ER) stress response is regarded as an important process in the aetiology of Alzheimer's disease (AD). The accumulation of pathogenic misfolded proteins and the disruption of intracellular calcium (Ca2+) signalling are considered to be fundamental mechanisms that underlie the induction of ER stress, leading to neuronal cell death. Indeed, a number of studies have proposed molecular mechanisms linking ER stress to AD pathogenesis based on results from in vitro systems and AD mouse models. However, stress responsivity was largely different between each mouse model, even though all of these models display AD-related pathologies. While several reports have shown elevated ER stress responses in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (Tg) AD mouse models, we and other groups, in contrast, observed no such ER stress response in APP-single-Tg or App-knockin mice. Therefore, it is debatable whether the ER stress observed in APP and PS1 double-Tg mice is due to AD pathology. From these findings, the roles of ER stress in AD pathogenesis needs to be carefully addressed in future studies. In this review, we summarize research detailing the relationship between ER stress and AD, and analyse the results in detail.
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页数:15
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