Although neurons account for most BACE1-mediated Aβ synthesis in AD, it has been demonstrated that inflammatory mediators, such as IFN-γ, TNF-α, and IL-1β, induce the expression of BACE1 and the release of Aβ in astrocytes, suggesting that these cells also contribute to the amyloidosis in AD [48, 51]. Here, IFNG is linked to Alzheimer disease.