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With various genetic and environmental risk factors, the accumulation of harmful amyloid plaques containing amyloid-\u03b2 (A\u03b2) peptides is one of the main hallmarks of AD. Recent findings show that the innate immune protein interferon-induced transmembrane protein 3 (IFITM3) binds to \u03b3-secretase and modulates A\u03b2 production, providing a direct link between neuroinflammation, amyloidogenesis, and the pathogenesis of AD. In this review, we explore IFITM3-mediated modulation of \u03b3-secretase complex activity and its pivotal role in AD pathology during neuroinflammation. 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