Pluta and Zhang et al. found that transient CI/R-induced site-specific hyperphosphorylated Tau and increased brain immunoreactivity to the N- and C-terminal of amyloid beta precursor protein (APP) and Aβ in the ischemic cortex, implying that cerebral ischemia is involved in the pathogenesis of AD and contributes to the development of AD after stroke [40, 41]. The gene discussed is APP; the disease is stroke disorder.