Vascular endothelial cell dysfunction and Alzheimer′s disease

Alzheimer′s disease (AD) is a neurodegenerative disease with complex pathological mechanism characterized by accumulation of amyloid plaques and neurofibrillary tangles in the brain. Increasing evidence suggests that vascular dysfunction due to endothelial cell injury may have a pathogenic role in the occurrence and development of AD. Malfunction of the bloodbrain barrier caused by endothelial cell dysfunction is associated with the accumulation of several neurotoxic molecules within brain parenchyma, a reduction in cerebral blood flow, amyloid-β transfer and hypoxia, especially at the early stages of the disease. At the same time, it cannot be ignored that the peripheral arterial vascular endothelial cell dysfunction also seems to be closely related to the risk and the severity of symptoms of AD. Some molecules are thought to be messengers connecting the central and peripheral endothelial cells. Peripheral and central vascular endothelial cells communicate with each other and influence the progression of AD through some common mechanisms. In this review, we provide an appraisal of the endothelial cell dysfunction in cerebral and systemic vasculature, and give the evidence that vascular pathology is inextricably linked to disease onset and progression of AD.