Although there is experimental and clinical evidence for some interaction between β- amyloid toxicity and ischemia, their either alone or combined effects on dynamic neurovascular coupling and the pathophysiology that leads to reduced cerebral blood flow (CBF) is largely unexplored. An in vivo sequential computed tomography imaging immediately after comorbid injury showed an acute drop in CBF and loss of established astrocytic-endothelium contacts, blood–brain barrier and neuronal loss. A time-dependent increase in glia cell numbers in ischemic rats was accompanied with restored blood brain-barrier damage and normalized CBF, four weeks after the injury. Delayed repair of BBB or impaired CBF observed in Abeta toxicity+ischemic rats compared to either injury was related to reduced number of glial cells. Astrocytic contact-independent recovery of BBB and CBF in the absence of neurons interpret the role of communication between astrocytes, microglia, and endothelial cells in ischemic rats.