Abstract
Newly emerged evidence reveals that ischemic stroke and Alzheimer's disease (AD) share pathophysiological changes in brain tissue including hypoperfusion, oxidative stress, immune exhaustion, and inflammation. A mechanistic link between hypoperfusion and amyloid β accumulation can lead to cell damage as well as to motor and cognitive deficits. This review will discuss decreased cerebral perfusion and other related pathophysiological changes common to both ischemic stroke and AD, such as vascular damages, cerebral blood flow alteration, abnormal expression of amyloid β and tau proteins, as well as behavioral and cognitive deficits. Furthermore, this review highlights current treatment options and potential therapeutic targets that warrant further investigation.