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(Stroke. 2009;40:2601.)
© 2009 American Heart Association, Inc.

Topical Reviews

β-Amyloid, Blood Vessels, and Brain Function

Eric E. Smith, MD, MPH Steven M. Greenberg, MD, PhD

From the Division of Neurology, Department of Clinical Neurosciences (E.E.S.), University of Calgary, Calgary, Alberta, Canada; and the Department of Neurology (S.M.G.), Hemorrhagic Stroke Research Program, and the Department of Neurology, Massachusetts General Hospital, Boston, Mass.

Correspondence to Steven M. Greenberg, MD, PhD, Kistler Stroke Research Center, 175 Cambridge Street, Suite 300, Boston, MA 02114. E-mail sgreenberg{at}partners.org

Philip Gorelick MD John V. Bowler MD Section Editors:

Cerebrovascular disease and Alzheimer disease are common diseases of aging and frequently coexist in the same brain. Accumulating evidence suggests that the presence of brain infarction, including silent infarction, influences the course of Alzheimer disease. Conversely, there is evidence that β-amyloid can impair blood vessel function. Vascular β-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble β-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli. In this review, we discuss current evidence linking β-amyloid metabolism with vascular function and morphological changes in animals and humans.

Key Words: Alzheimer disease • cerebral amyloid angiopathy • vascular cognitive impairment