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(Stroke. 2004;35:2616.)
© 2004 American Heart Association, Inc.
Articles |
From the Neurology Clinical Trials Unit and Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass.
Correspondence to Dr Steven M. Greenberg, Wang ACC 836, Massachusetts General Hospital, Boston, MA 02114. E-mail sgreenberg{at}partners.org
We review accumulating evidence that cerebrovascular amyloid deposition (cerebral amyloid angiopathy [CAA]) is an independent risk factor for cognitive dysfunction. The two population-based autopsy studies that have analyzed cognitive status during life as a function of CAA have each suggested deleterious effects of CAA on cognition even after controlling for age and Alzheimer disease pathology. We also review data from patients with CAA-related intracerebral hemorrhage (the one form of CAA that can be noninvasively recognized) suggesting associations of CAA with radiographic white matter abnormalities and cognitive impairment. These data highlight the importance of elucidating the effects of vascular amyloid on cerebrovascular function and of developing therapeutic strategies for this potentially widespread form of microvascular cognitive impairment.
Key Words: amyloid angiopathy vascular dementia
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