Lastly, our group has shown, in multiple studies, that intracerebroventricular (i.c.v) injections of Aβ1–42 increased GFAP, inflammatory markers, e.g., nuclear factor-κB (NFκB) TNFα, IL-1β, and oxidative stress markers, e.g., nuclear factor erythroid-related factor 2 (Nrf2) and heme oxygenase 1 (HO1), which indicated that AD-associated pathology also increase astrocyte activity and promote inflammation [66,67,68,69]. This evidence concerns the gene GFAP and Alzheimer disease.