2022 Volume 59 Issue 1 Pages 151-156
Alzheimer’s disease (AD) is thought to be triggered by abnormal deposition of amyloid β (Aβ) around neurons in the brain parenchyma. Recently, cerebrovascular disorders, such as transient cerebral ischemia, have also been considered as a risk factor of AD. Neurons in the brain are vulnerable to ischemia; however, stimulation of vasodilating nerves mitigates the degree of ischemia and consequently reduces the number of damaged neurons. Thus, the cerebrovascular reaction during ischemia presumably contributes to the pathophysiology of AD. Aβ also deposits around the pial artery running over the brain surface, as well as in the brain parenchyma. In the present mini-review, we discuss the influence of Aβ deposition on cerebrovascular functions including our recent findings.