Affiliations: [a] Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China
| [b] Department of Neurology, Nanjing Yuhua Hospital, Nanjing, China
| [c] School of Basic Medicine & Clinical Pharmacy, China Pharmaceutical University, Nanjing, China
Correspondence:
[*]
Correspondence to: Prof. Teng Jiang and Prof. Ying-Dong Zhang, No. 68 Changle Road, Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China, 210006. Tel.: +86 25 52271000; E-mail: jt870918@163.com. (Jiang); E-mail: zhangyingdong@aliyun.com. (Zhang).
Note: [1] These authors contributed equally to this work.
Abstract: Late-onset Alzheimer’s disease (AD) accounts for most of all AD casesand is currently considered a complex disorder caused by a combination of environmental and genetic factors. As an important family member of triggering receptor expressed on myeloid cells (TREM), TREM-like transcript 2 gene (TREML2) locates on human chromosome 6p21.1, a newly-identified hot zone for AD susceptibility, and encodes atransmembrane immune receptor. Emerging evidence implied a potential role of TREML2 in the susceptibility and pathogenesis of AD. Here, we review the recent literature about the association of TREML2 variants with AD risk and disease endophenotypes. Moreover, we summarize the latest findings regarding cellular localization and biological functions of TREML2 and speculate its possible role in AD pathogenesis. In addition, we discuss future research directions of TREML2 and AD.
