Abstract

This year’s Princeton conference featured a session on vascular cognitive impairment (VCI), signaling recognition, a long time in coming, of this important consequence of cerebrovascular disease. The emphasis was on cerebrovascular dysregulation and small vessel white matter disease, drawing from animal models, human pathology, neuroimaging, epidemiology, and the recent clinical trial in CADASIL, as summarized below. Cerebrovascular oxidative stress from reactive oxygen species mediated by NADPH oxidase present in cerebral vessels may be the final common pathway of the cerebrovascular dysregulation induced by aging, Alzheimer disease (AD), and hypertension, according to Iadecola and colleagues.1 Cerebral energy demands are serviced through control mechanisms such as functional hyperemia and cerebrovascular autoregulation, which tailor the blood supply to tissue needs and maintain perfusion over a wide range of blood pressures. Aging changes the structure and vasodilatory capacity of vessels, increasing susceptibility to ischemia. Chronic hypertension induces remodeling and stenosis of the arteries and fibrinoid necrosis of the arterioles, …

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