Through genetic abrogation of type-I IFN signalling by targeting its receptor IFNAR1, we identify that IFNAR1−/− primary microglia exhibit a decreased IL1β, IL6 and TNFα response to monomeric Aβ1–42, and that targeting IFNAR1 within primary microglia isolated from the APPswePS1ΔE9 AD model leads to an enhanced ability to phagocytose FITC Aβ1–42. This evidence concerns the gene IFNAR1 and Alzheimer disease.