In particular, the presence of active caspases in the brain vasculature (254, 256, 261), accompanied by the discussed evidence of tau transmission within neurovascular cells, supports the hypothesis that caspase activation may induce accumulation of toxic caspase-3 cleaved tau in cerebrovascular and glial cells, thus precipitating neurovascular pathology in AD, CAA, and tauopathies. This evidence concerns the gene CASP3 and Alzheimer disease.