Interestingly, an experimental study has demonstrated that pericyte loss in mice overexpressing Swedish human APP (APPsw/0/Pdgfr+/−) aggravates AD-related pathology mainly by increasing brain soluble Aβ levels, which in turn self-amplifies Aβ-induced pericyte loss, thus exacerbating cerebral microvascular damage and cognitive impairments [31]. The gene discussed is APP; the disease is Alzheimer disease.