title: Cerebral amyloid angiopathy and vessel dysfunction.
abstract: Cerebral amyloid angiopathy (CAA), defined by deposition of the beta-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 beta-amyloid may alter vessel physiology. Future studies will seek to define the clinical importance of vascular beta-amyloid as a potential target for drug therapy in dementia.
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Boston, Mass 02114, USA. greenberg@helix.mgh.harvard.edu
authors.forename: Steven M
authors.initials: SM
authors.lastname: Greenberg
mesh_terms: D000368:Aged; D000818:Animals; D001808:Blood Vessels / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D016657:Cerebral Amyloid Angiopathy / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000235:genetics / Q000502:physiology*; D006801:Humans; D051379:Mice