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Published Online
on May 14, 2009

Stroke. 2009
Published online before print May 14, 2009, doi: 10.1161/STROKEAHA.108.536839
A more recent version of this article appeared on July 1, 2009
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Submitted on September 10, 2008
Revised on November 22, 2008
Accepted on December 1, 2008

{beta}-Amyloid, Blood Vessels, and Brain Function

Eric E. Smith MD, MPH and 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.

* To whom correspondence should be addressed. E-mail: sgreenberg{at}partners.org.

Abstract—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 {beta}-amyloid can impair blood vessel function. Vascular {beta}-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 {beta}-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli. In this review, we discuss current evidence linking {beta}-amyloid metabolism with vascular function and morphological changes in animals and humans.


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