While the mechanism of BACE1 elevation in AD and APP Tg brains is not fully understood, recent data indicate that BACE1 levels are upregulated during stresses associated with AD risk such as energy deprivation [22], [27], hypoxia and stroke [28]–[30], oxidative stress [31] and traumatic brain injury [32], [33]. The gene discussed is BACE1; the disease is stroke disorder.