A role for increased IFN-Is in AD pathogenesis (rather than just being a bystander effect) has been demonstrated in mouse models, where IFNAR1 deletion or neutralization resulted in downregulated expression of proinflammatory cytokines, attenuated microgliosis, increased complement-mediated synapse engulfment, enhanced astrogliosis, and partial improvement in learning (43, 79, 125). Here, IFNAR1 is linked to Alzheimer disease.