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, rs6910730(G), is reported to associate with AD pathology; however, the exact mechanism is not yet clear. Since phagocytosis of A beta by monocytes enhances A beta clearance and attenuates AD pathogenesis, Jiang et al. has investigated if TREM1 can modulate A beta phagocytosis and degradation by monocytes in the central nervous system (CNS). They found that TREM1 facilitates microglial A beta phagocytosis while rs6910730(G) impairs this function and exacerbates AD pathogenesis. These findings suggest that TREM1 can be implemented investigated as a potential therapeutic target in AD.