Abstract
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 asa potential therapeutic target in AD.
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