Abstract
Aortic stiffness increases with age and is a robust predictor of cerebrovascular events and cognitive decline including Alzheimer's disease and other forms of dementia. Recent clinical studies have investigated the association between proximal aortic stiffness and pulsatile energy transmission that has deleterious effects on the cerebrovascular network in order to identify potential therapeutic targets. Aging causes disproportionate stiffening of the aorta compared with the carotid arteries, reducing protective impedance mismatches at their interface, increasing the transmission of destructive pulsatile pressure and energy to the cerebral circulation, and leading to cerebral small vessel disease. Thus, aortic stiffening and high-flow pulsatility are associated with alterations in the microvasculature of the brain, vascular endothelial dysfunction, and white matter damage, which contribute to impaired memory function with advancing age. Previous studies have also shown that silent lacunar infarcts and white matter hyperintensities are strongly associated with arterial stiffness. More and more evidence suggests that vascular etiologies, including aortic stiffness, impedance match, and microvascular damage, are associated with cognitive impairment and the pathogenesis of dementia. The measurement of arterial flow and pressure can help understand pulsatile hemodynamics and its impact on vital organs. Interventions that reduce aortic stiffness, such as improvement of the living environment, management of risk factors, and innovation and development of novel drugs, may reduce the risk for dementia.