| Apolipoprotein E genotype and cerebral amyloid angiopathy-related hemorrhage. | |
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MedLine Citation:
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PMID: 10818505 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Following the identification of the role of the apolipoprotein E (APOE) gene polymorphism in Alzheimer's disease (AD), this gene was examined in cerebral amyloid angiopathy (CAA). As in AD, the APOE epsilon 4 allele was found to be associated with CAA. Lobar intracerebral hemorrhage is the major clinical manifestation of CAA. Initial studies on a small number of patients with CAA-related hemorrhage (CAAH) identified overrepresentation of APOE epsilon 4. However, it became clear that confounding bias from concomitant AD and the need for pathologically confirmed cases of CAAH would also have to be considered. A larger series of pathologically confirmed cases of CAAH, also assessed for AD pathology, found a surprising overrepresentation of the APOE epsilon 2 allele. Because of the association between CAA and AD, it might have been predicted that patients with CAAH would have a low, rather than a high, epsilon 2 frequency. The overrepresentation of APOE epsilon 2 was present both in patients with and without AD, whereas a high epsilon 4 frequency correlated with concomitant AD. Further studies found that overrepresentation of APOE epsilon 2 is specific for CAAH and is not found in intracranial hemorrhages due to other causes. In CAAH, APOE epsilon 2 may interact with putative risk factors for hemorrhage, including antiplatelet/anticoagulant medication, minor head trauma, and hypertension. Several microvascular abnormalities in amyloid-laden blood vessels have been assumed to antedate CAAH and increase its likelihood. APOE epsilon 2 has now been found to be associated with some of these vascular abnormalities, specifically a "double-barrel" appearance and fibrinoid necrosis. The currently favored interpretation is that APOE epsilon 4 enhances deposition of amyloid-beta protein in the walls of cerebral blood vessels, whereas epsilon 2 is a risk factor for hemorrhage from amyloid-laden blood vessels by promoting specific "CAA-associated vasculopathies." |
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Authors:
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M O McCarron; J A Nicoll |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Annals of the New York Academy of Sciences Volume: 903 ISSN: 0077-8923 ISO Abbreviation: Ann. N. Y. Acad. Sci. Publication Date: 2000 Apr |
Date Detail:
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Created Date: 2000-06-02 Completed Date: 2000-06-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7506858 Medline TA: Ann N Y Acad Sci Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 176-9 Citation Subset: IM |
Affiliation:
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Department of Neuropathology, University of Glasgow, Southern General Hospital NHS Trust, United Kingdom. mmc18f@clinmed.gla.ac.uk |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alzheimer Disease
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genetics Apolipoprotein E2 Apolipoprotein E4 Apolipoproteins E / genetics* Cerebral Amyloid Angiopathy / complications, genetics* Cerebral Hemorrhage / etiology, genetics* Genotype Humans Risk Factors |
| Chemical | |
Reg. No./Substance:
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0/Apolipoprotein E2; 0/Apolipoprotein E4; 0/Apolipoproteins E |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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