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(Stroke. 2009;40:S38.)
© 2009 American Heart Association, Inc.

Vascular Cognitive Impairment

Vascular Cognitive Impairment: Small Vessels, Big Toll

Introduction

From the Heart and Stroke Foundation Centre for Stroke Recovery and Departments of Medicine (Neurology) (S.B.), Sunnybrook Health Sciences Centre, University of Toronto, Canada; and the Division of Neurobiology, Department of Neurology and Neuroscience (C.I.), Weill Medical College of Cornell University, NY.

Correspondence to Sandra E. Black, MD, FRCP(C), Brill Professor of Neurology, Department of Medicine, Cognitive Neurology, A421, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON M4N 3M5. E-mail sandra.black@sunnybrook.ca

Key Words: vascular cognitive impairment • oxidative stress • hypertension • aging • Alzheimer disease • venous collagenosis • diabetes • CADASIL

An extract of the first 250 words of the full text is provided, because this article has no 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, alters cerebrovascular reactivity, and shifts autoregulation to the right, increasing vulnerability to hypotension, as well as attenuating functional hyperemia. Amyloid beta (Aβ), the peptide produced in toxic amounts in AD, is also vasculopathic, disrupting vascular endothelium and myocytes, obliterating capillaries and, likewise, impairing functional hyperemia and autoregulation. Fibrillar Aβ deposits around arterioles, weakens the muscular wall, and conduces both to hemorrhage and occlusion. These vasculopathic effects of aging, hypertension, and Aβ, acting alone or in concert, lead to hypoperfusion, blood brain barrier dysfunction, compromised protein synthesis and synaptic plasticity, and eventually neuronal death with cognitive . . . [Full Text of this Article]