Cerebrovascular Dysfunction at the Intersection of Ischemia and Alzheimer’s Disease

Cerebrovascular dysregulation is one of the earliest detectable changes in Alzheimer’s disease (AD) etiology that precedes the descent into dementia1. Ischemic events such as stroke and silent infarcts trigger cerebrovascular dysfunction2,3, accelerate cognitive decline4 and increase dementia risk5. Further, the resulting decrease in cerebral blood flow (CBF) can induce the formation of amyloid β6. Thus, we examined cerebrovascular function at the intersection of ischemia and AD by measuring CO2‐evoked hyperemia and neurovascular coupling (NVC) after small strokes in wild type and Tg2576 model of AD‐related amyloidosis.