In the TgCRND8 mouse model of AD (overexpression of human KM670/671NL Swedish and V717F Indiana mutant APP), the depletion of PVMs exacerbated CAA severity, resulting in a significant increase in thioflavin S-positive cortical blood vessels and selective accumulation of Aβ42 peptides in the vasculature [56]. The gene discussed is APP; the disease is Alzheimer disease.