To examine whether inhibiting reactive astrocyte-derived S100B might impact progression of AD-like pathology in the Tg2576 AD mouse model [127], we orally administered the S100B biosynthesis blocker, arundic acid, to Tg2576 mice for 6 months, commencing at 12 months of age (when β-amyloid plaques are initially present in this AD mouse model). This evidence concerns the gene S100B and Alzheimer disease.