APP and Alzheimer disease: However, co-stimulation of primary human astrocytes in culture with IFN-γ and TNF-α induced Aβ production, and deletion of the IFN-γ receptor reduced gliosis and amyloid plaque deposition in APP transgenic mice, which would suggest elevated levels of inflammation within the CNS exacerbates AD pathology (Blasko et al., 2000; Yamamoto et al., 2007).