Cerebral Amyloid Angiopathy and Vessel Dysfunction

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Abstract
Cerebral amyloid angiopathy (CAA), defined by deposition of the β-amyloid peptide in medium and small cortical and meningeal vessels, is a well-recognized cause of hemorrhagic stroke. This paper reviews the accumulating evidence supporting an additional role for CAA in producing vessel dysfunction, reduced cerebral blood flow and ischemia. Ischemic lesions are characteristic of several hereditary CAA syndromes, including a recently described mutation of the amyloid precursor protein associated with dementia (but not hemorrhagic stroke) in an Iowa family. Ischemic lesions are seen in some sporadic CAA patients as well, and recent data from transgenic mice suggest potential mechanisms by which β-amyloid may alter vessel physiology. Future studies will seek to define the clinical importance of vascular β-amyloid as a potential target for drug therapy in dementia.