Close encounter: mitochondria, endoplasmic reticulum and Alzheimer's disease

被引：17

作者：

De Strooper, Bart ^{[1
]}

Scorrano, Luca ^{[2
]}

机构：

[1] KuLeuven, VIB, VIB Ctr Biol Dis, Ctr Human Genet, Louvain, Belgium

[2] Univ Geneva, Sch Med, Dept Cell Physiol & Metab, CH-1211 Geneva, Switzerland

来源：

EMBO JOURNAL | 2012年 / 31卷 / 21期

关键词：

DYSFUNCTION; MEMBRANE;

D O I：

10.1038/emboj.2012.279

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 characterized by the loss of hippocampal and cortical neurons as a consequence of the accumulation of amyloid-beta (A beta). A beta is produced from the amyloid precursor protein (APP) by the gamma-secretase complex components presenilin-1 (PS1) and -2 (PS2), which are mutated in genetic forms of AD. In this issue, Schon and coworkers show that PS1 and PS2 are located at the interface between mitochondria and endoplasmic reticulum (ER). In models of familial and sporadic AD, these two organelles are juxtaposed closely, affecting shared lipid metabolic pathways. The interface between mitochondria and ER emerges as a new potential determinant of AD pathogenesis.

引用

页码：4095 / 4097

页数：3

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