TREM2 dependent and independent functions of microglia in Alzheimer's disease

被引：89

作者：

Hou, Jinchao ^{[1
]}

Chen, Yun ^{[1
,2
]}

Grajales-Reyes, Gary ^{[1
]}

Colonna, Marco ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA

来源：

MOLECULAR NEURODEGENERATION | 2022年 / 17卷 / 01期

基金：

美国国家卫生研究院; 中国国家自然科学基金;

关键词：

Alzheimer's disease; Beta-amyloid pathology; Tauopathy; Demyelination; Microglia; TREM2; APOE; NLRP3 INFLAMMASOME ACTIVATION; INNATE IMMUNE RECEPTOR; AMYLOID-BETA; MOUSE MODEL; CEREBROSPINAL-FLUID; APOLIPOPROTEIN-E; TRANSGENIC MICE; CODING VARIANTS; SOLUBLE TREM2; BRAIN;

D O I：

10.1186/s13024-022-00588-y

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Microglia are central players in brain innate immunity and have been the subject of extensive research in Alzheimer's disease (AD). In this review, we aim to summarize the genetic and functional discoveries that have advanced our understanding of microglia reactivity to AD pathology. Given the heightened AD risk posed by rare variants of the microglial triggering receptor expressed on myeloid cells 2 (TREM2), we will focus on the studies addressing the impact of this receptor on microglia responses to amyloid plaques, tauopathy and demyelination pathologies in mouse and human. Finally, we will discuss the implications of recent discoveries on microglia and TREM2 biology on potential therapeutic strategies for AD.

引用

页数：19

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