期刊
MECHANISMS OF AGEING AND DEVELOPMENT
卷 195, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2021.111438
关键词
TREM2; Microglia; Alzheimer's disease; Brain homeostasis
资金
- Capital's Funds for Health Improvement and Research [CFH 2020-4-1033]
- Capital Medical University Funding [PYZ19137]
- Beijing Natural Science Foundation [JQ19024]
- National Natural Science Foundation of China [81671040, 81970996]
TREM2 plays a crucial role in the pathogenesis of Alzheimer's disease (AD), influencing microglial functions in amyloid and tau pathologies, inflammatory responses, and metabolism. It may act alone or with other molecules such as apolipoprotein E (APOE) as a multifaceted player in microglial functions.
Triggering receptor expressed on myeloid cells 2 (TREM2) has been suggested to play a crucial role in Alzheimer's disease (AD) pathogenesis, as revealed by genome-wide association studies (GWAS). Since then, rapidly increasing literature related to TREM2 has focused on elucidating its role in AD pathology. In this review, we summarize our understanding of TREM2 biology, explore TREM2 functions in microglia, address the multiple mechanisms of TREM2 in AD, and raise key questions for further investigations to elucidate the detailed roles and molecular mechanisms of TREM2 in microglial responses. A major breakthrough in our understanding of TREM2 is based on our hypothesis suggesting that TREM2 may act as a multifaceted player in microglial functions in AD brain homeostasis. We conclude that TREM2 can not only influence microglial functions in amyloid and tau pathologies but also participate in inflammatory responses and metabolism, acting alone or with other molecules, such as apolipoprotein E (APOE). This review provides novel insight into the broad role of TREM2 in microglial function in AD and enables us to develop new strategies aimed at the immune system to treat AD pathogenesis.
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