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A systematic review of the role of TREM2 in Alzheimer's diseaseOACSTPCDMEDLINE

A systematic review of the role of TREM2 in Alzheimer's disease

英文摘要

Background:Given the established genetic linkage between triggering receptors expressed on myeloid cells 2(TREM2)and Alzheimer's disease(AD),an expanding research body has delved into the intricate role of TREM2 within the AD context.However,a conflicting landscape of outcomes has emerged from both in vivo and in vitro investigations.This study aimed to elucidate the multifaceted nuances and gain a clearer comprehension of the role of TREM2. Methods:PubMed database was searched spanning from its inception to January 2022.The search criteria took the form of("Alzheimer's disease"OR"AD")AND("transgenic mice model"OR"transgenic mouse model")AND("Triggering receptor expressed on myeloid cells"OR"TREM2").Inclusion criteria consisted of the following:(1)publication of original studies in English;(2)utilization of transgenic mouse models for AD research;and(3)reports addressing the subject of TREM2. Results:A total of 43 eligible articles were identified.Our analysis addresses four pivotal queries concerning the interrelation of TREM2 with microglial function,Aβ accumulation,tau pathology,and inflammatory processes.However,the diverse inquiries posed yielded inconsistent responses.Nevertheless,the inconsistent roles of TREM2 within these AD mouse models potentially hinge upon factors such as age,sex,brain region,model type,and detection methodologies. Conclusions:This review substantiates the evolving understanding of TREM2's disease progression-dependent impacts.Further-more,it reviews the interplay between TREM2 and its effects across diverse tissues and temporal stages.

Yunsi Yin;Hanchen Yang;Ruiyang Li;Guangshan Wu;Qi Qin;Yi Tang

Department of Neurology & Innovation Center for Neurological Disorders,Xuanwu Hospital,Capital Medical University,National Center for Neurological Disorders,Beijing 100053,China

TREM2;Alzheimer's disease;Mouse model;Microglia;Amyloid-β accumulation;Tau pathology;Inflammation

《中华医学杂志(英文版)》 2024 (014)

1684-1694 / 11

This work was supported by grants from National Nat-ural Science Foundation of China(Nos.82220108009,81970996,and 82201568),National Key Research and Development Program of China(No.2022YFC3602600),STI2030-Major Projects(No.2021ZD0201801),Young Elite Scientists Sponsorship Program by CAST(No.2021QNRC001),Beijing Hospitals Authority Innovation Studio of Young Staff Funding Support(No.202118),and Beijing Nova Program(No.Z211100002121051).

10.1097/CM9.0000000000003000

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