Chronic cerebral hypoperfusion and dementia

Abstract

Abstract“Cerebral small vessel disease” is a general term featuring a group of disease conditions with characteristic lesions affecting mainly small vessels in the brain, such as Binswanger's disease, leukoaraiosis and lacunar infarctions. Cerebral small vessels consist of a series of blood vessels, which originate from the pial arteries on the surface of the brain, and branch into arterioles, capillaries and postcapillary venules. Each of the blood vessels has a distinct structure and function. The blood–brain barrier, which does not exist in the other organs, functions in the brain. Dysfunction of the blood–brain barrier is thought to be a major cause of cerebral small vessel diseases. Recent findings have shown that maintenance of the blood–brain barrier is kept by various types of cells, such as vascular endothelial cells, astrocytes and pericytes, which work collaboratively as a neurovascular unit. Currently, larger vessels at the arteriolar level have been studied intensively; however, the pathological condition of the neurovascular unit at the capillary level still needs to be elucidated. The bilateral carotid artery stenosis model simulates chronic cerebral hypoperfusion, formation of white matter lesions and cognitive impairments seen in humans. Using this model, we found microcirculation disturbance especially in the postcapillary venule, and postulated it as a final step leading to white matter lesions and cognitive impairment. Taken together, we suggest that chronic cerebral hypoperfusion plays a pivotal role in the pathogenesis of cerebral small vessel diseases.