The activity of γ-secretase is critical to the pathogenesis of Alzheimer's disease (AD). How its activity is regulated is intriguing and highly important for any AD therapy that focuses on reduction of toxic amyloid peptides and amyloid deposition in patients. Recently, interferon-induced transmembrane protein 3 (IFITM3) has been identified as a novel regulator of γ-secretase through a specific interaction. This commentary highlights this exciting study and provides an updated link of γ-secretase activity to innate immunity through IFITM3.
Keywords: Alzheimer’s disease; Amyloid plaques; IFITM3; Innate immunity; Interferon-induced transmembrane protein; Nicastrin; Photo-crosslinking; Presenilin; Γ-secretase.