The results discussed above using an in vivo genetic approach can be interpreted as definitive evidence that forced expression of human S100B exacerbates AD-like pathology, including brain parenchymal and cerebral vascular β-amyloid deposits, Aβ levels, β-amyloid deposit-associated astrocytosis and microgliosis, and pro-inflammatory cytokines [138]. Here, S100B is linked to Alzheimer disease.