Source:http://linkedlifedata.com/resource/pubmed/id/10505604
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1999-12-2
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pubmed:abstractText |
Several studies have demonstrated genetic associations between Alzheimer's disease (AD) and polymorphisms in the promoter/enhancer regions of the apolipoprotein E (APOE) gene. These studies raise the possibility that APOE transcription control may be involved in altered risks for AD. We evaluated polymorphic sites in the intron-1 enhancer element (IE-1G/C) and in the APOE promoter (-219G/T). For the IE-1 polymorphism, we analyzed 433 individuals (183 AD and 250 controls), and found a strong linkage between the IE-1G allele and APOE-epsilon4. When we controlled for this linkage using log-linear model analysis, we found no independent association between the IE-1 polymorphism and AD. For the -219 polymorphism, we analyzed 475 individuals (168 AD cases, 234 controls, and 73 cases of cerebral amyloid angiopathy (CAA)). We found strong linkages between the -219G allele and APOE-epsilon2 and between the -219 T allele and APOE-epsilon4. Controlling for these linkages, we found no independent association between the -219 polymorphism and AD or CAA. Thus, our studies do not support independent associations between AD and either the IE-1 or the -219 polymorphisms.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein E2,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein E4,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0304-3940
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
17
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pubmed:volume |
272
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
155-8
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:10505604-Alleles,
pubmed-meshheading:10505604-Alzheimer Disease,
pubmed-meshheading:10505604-Apolipoprotein E2,
pubmed-meshheading:10505604-Apolipoprotein E4,
pubmed-meshheading:10505604-Apolipoproteins E,
pubmed-meshheading:10505604-Cerebral Amyloid Angiopathy,
pubmed-meshheading:10505604-DNA,
pubmed-meshheading:10505604-DNA Primers,
pubmed-meshheading:10505604-Genetic Linkage,
pubmed-meshheading:10505604-Humans,
pubmed-meshheading:10505604-Introns,
pubmed-meshheading:10505604-Polymorphism, Genetic,
pubmed-meshheading:10505604-Promoter Regions, Genetic,
pubmed-meshheading:10505604-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:10505604-Risk Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Lack of independent associations of apolipoprotein E promoter and intron 1 polymorphisms with Alzheimer's disease.
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pubmed:affiliation |
Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA. rebeck@helix.mgh.harvard.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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