Saadipour Khalil
Department of Cell Biology, Physiology & Neuroscience, Skirball Institute of Bimolecular Medicine, New York University Langone Medical Center, New York, NY, 10016, USA.
Neurotox Res. 2017 Jul;32(1):14-16. doi: 10.1007/s12640-017-9716-y. Epub 2017 Mar 11.
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, 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 rs6910730 impairs this function and exacerbates AD pathogenesis. These findings suggest that TREM1 can be implemented investigated as a potential therapeutic target in AD.
免疫被认为在阿尔茨海默病(AD)的发病机制中起关键作用。髓系细胞触发受体-1(TREM1)是免疫球蛋白超家族受体的成员,在单核细胞和小胶质细胞中广泛表达。另一方面,据报道TREM1变体rs6910730与AD病理相关;然而,确切机制尚不清楚。由于单核细胞对Aβ的吞噬作用增强了Aβ清除并减轻了AD发病机制,Jiang等人研究了TREM1是否可以调节中枢神经系统(CNS)中单核细胞对Aβ的吞噬和降解。他们发现TREM1促进小胶质细胞对Aβ的吞噬,而rs6910730损害这一功能并加剧AD发病机制。这些发现表明,TREM1可以作为AD潜在的治疗靶点进行研究。