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46 reviewsSUMMARYThe progression of Alzheimer’s disease (AD) involves temporal dynamics of microglial activation. Restoringor maintaining microglial homeostasis has emerged as a promising therapeutic strategy to combat AD.Transmembrane protein 119 (TMEM119) is a homeostatic marker of microglia but has not been fully studiedunder AD pathological conditions. Here, we observed that amyloid-beta (Aβ) induced a decrease in TMEM119expression in microglia, and TMEM119 deficiency increased AD progression in the 5×FAD mouse model.TMEM119 bound to Aβ oligomers and recruited low-density lipoprotein receptor 1, which in turn degradedTMEM119 itself. Overexpression of TMEM119 in microglia enhanced their phagocytic activity and alleviatedcognitive deficits in 5xFAD mice. Administration of the small molecules Kartogenin and SRI-011381, whichwe found enhanced TMEM119 expression, substantially promoted Aβ clearance and improved cognitivefunction in AD mice, even during the mid-stage of the disease. These findings identify TMEM119 as a promising therapeutic target for AD.
