The development of neuronal death and amyloid plaques is a characteristic feature of ischemic- and Alzheimer-type dementia. An important aspect of neuronal loss and amyloid plaques are their topography and neuropathogenesis. This review was performed to present the hypothesis that different fragments of blood-borne amyloid precursor protein are able to enter the ischemic blood-brain barrier. Chronic disruption of the blood-brain barrier after ischemic injury was shown. As an effect of chronic ischemic blood-brain barrier injury, a visible connection of amyloid plaques with neurovasculature was observed. This neuropathology appears to have similar distribution and mechanisms to Alzheimer's disease. The usefulness of rival ischemic theory in elucidating the neuropathogenesis of amyloid plaques formation and neuronal death in Alzheimer's disorder is discussed.