TREM1: A Potential Therapeutic Target For Alzheimer’s Disease
Immunity has been suggested to play crucial roles in the pathogenesis of Alzheimer’s disease (AD). The triggering receptor expressed on myeloid cells-1 (TREM1), a member of the immunoglobulin superfamily of receptors, is widely expressed in monocytes and microglia. On the other hand, TREM1 variant, rs6910730G, is reported to associate with AD pathology; however, the exact mechanism is not yet clear. Since phagocytosis of Aβ by monocytes enhances Aβ clearance and attenuates AD pathogenesis, Jiang et al. has investigated if TREM1 can modulate Aβ phagocytosis and degradation by monocytes in the central nervous system (CNS). They found that TREM1 facilitates microglial Aβ phagocytosis while rs6910730G impairs this function and exacerbates AD pathogenesis. These findings suggest that TREM1 can be implemented investigated as a potential therapeutic target in AD.
KeywordsTREM1 rs6910730G Microglia Phagocytosis Amyloid beta Alzheimer’s disease
- Benitez BA, Cooper B, Pastor P, Jin SC, Lorenzo E, Cervantes S et al (2013) TREM2 is associated with the risk of Alzheimer’s disease in Spanish population. Neurobiol Aging 34(1711):e1715–e1717Google Scholar
- Cuyvers E, Bettens K, Philtjens S, Van Langenhove T, Gijselinck I, van der Zee J et al (2014) Investigating the role of rare heterozygous TREM2 variants in Alzheimer’s disease and frontotemporal dementia. Neurobiol Aging 35(726):e711–e729Google Scholar
- Jiang T, Tan L, Chen Q, Tan MS, Zhou JS, Zhu XC et al (2016a) A rare coding variant in TREM2 increases risk for Alzheimer’s disease in Han Chinese. Neurobiol Aging 42(217):e211–e213Google Scholar
- Jiang T, Zhang YD, Gao Q, Zhou JS, Zhu XC, Lu H, et al. (2016b). TREM1 facilitates microglial phagocytosis of amyloid beta. Acta neuropathologicaGoogle Scholar