The predisposition to Alzheimer’s disease (AD) (mainly due to triplication of the gene encoding for APP [40, 77]) and the chronic hyperactivity of the interferon system (primarily due to triplication of genes encoding for interferon receptor subunits IFNAR1, IFNAR2, and IFNGR2, IL10RB, and interferon-stimulated genes MX1and MX2 [61, 134]) may contribute to the increased rate of neurological symptoms in DS individuals who contracted the virus [62]. This evidence concerns the gene IFNAR2 and early-onset autosomal dominant Alzheimer disease.