Abstract
Several genes in innate immunity have been implicated in Alzheimer's disease (AD). However, the effect of innate immunity on amyloid β (Aβ) production, which makes amyloid plaques in AD brains, was previously not known. Recently, the antiviral protein interferon-induced transmembrane protein 3 (IFITM3) has been identified as a novel γ-secretase modulatory protein for Aβ production. In this review, the mechanisms of how innate immunity modulates Aβ production via IFITM3-γ-secretase complexes and contributes to AD pathogenesis are discussed.
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