TREM2 variants: new keys to decipher Alzheimer disease pathogenesis

被引：312

作者：

Colonna, Marco ^{[1
]}

Wang, Yaming ^{[2
]}

机构：

[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63108 USA

[2] Eli Lilly & Co, Lilly Corp Ctr, Indianapolis, IN 46285 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2016年 / 17卷 / 04期

基金：

美国国家卫生研究院;

关键词：

MYELOID CELLS 2; GENOME-WIDE ASSOCIATION; APOLIPOPROTEIN-E; OSTEOCLAST DIFFERENTIATION; DAP12-ASSOCIATED RECEPTOR; FRONTOTEMPORAL DEMENTIA; MICROGLIAL RESPONSE; IDENTIFIES VARIANTS; COMMON VARIANTS; UP-REGULATION;

D O I：

10.1038/nrn.2016.7

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2)-an immune receptor that is found in brain microglia-as risk factors for non-familial Alzheimer disease (AD). Furthermore, animal studies have indicated that microglia have an important role in the brain response to amyloid-beta(A beta) plaques and that TREM2 variants may have an impact on such a function. We discuss how TREM2 may control the microglial response to A beta and its impact on microglial senescence, as well as the interaction of TREM2 with other molecules that are encoded by gene variants associated with AD and the hypothetical consequences of the cleavage of TREM2 from the cell surface.

引用

页码：201 / 207

页数：7

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