PMC-12 treatment prevented Aβ-induced increases in both AD-related neuropathological markers (Aβ, Iba-1, and GFAP) and inflammatory mediators (iNOS, COX-2, IL-1β, IL-6, TLR-2, and TLR-4) as well as in learning and spatial memory deficits in Aβ-treated mice. The gene discussed is GFAP; the disease is Alzheimer disease.