Linked Life Data

11901242

Source:http://linkedlifedata.com/resource/pubmed/id/11901242

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-3-19
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1015-9770
pubmed:author
pubmed:copyrightInfo
Copyright 2002 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
13 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
42-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Cerebral amyloid angiopathy and vessel dysfunction.
pubmed:affiliation
Department of Neurology, Massachusetts General Hospital, Boston, Mass 02114, USA. greenberg@helix.mgh.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review