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Article: Absence of association between Alzheimer disease and the -491 regulatory region polymorphism of APOE

TitleAbsence of association between Alzheimer disease and the -491 regulatory region polymorphism of APOE
Authors
Song, YQRogaeva, EPremkumar, SBrindle, NKawarai, TOrlacchio, AYu, GLevesque, GNishimura, MIkeda, MPei, YO'Toole, CDuara, RBarker, WSorbi, SFreedman, MFarrer, LSt GeorgeHyslop, P
Keywords-491 A/T polymorphism
Alzheimer disease
APOE ε2/ε3/ε4 polymorphism
Issue Date1998
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 1998, v. 250 n. 3, p. 189-192 How to Cite?
DOI: http://dx.doi.org/10.1016/S0304-3940(98)00470-4
AbstractA novel polymorphism (-491 A/T) within the regulatory region on the apolipoprotein E gene has recently been reported to be associated with risk for Alzheimer disease (AD). To test this association in an independent data set, we have examined this polymorphism in a sample of 88 well-characterized AD cases and compared the allele frequency and genotype frequencies for this polymorphism with those observed in 112 cegnitively normal subjects drawn from the same ethnic group. These results suggest that in the current data set at least, the -491 NT polymorphism is not associated with risk for AD, but may be in partial linkage disequilibrium with the APOE ε2/ε3/ε4 polymorphism.
Persistent Identifierhttp://hdl.handle.net/10722/134744
ISSN
0304-3940
2023 Impact Factor: 2.5
2023 SCImago Journal Rankings: 0.745
ISI Accession Number ID
WOS:000075092500013
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorSong, YQen_HK
dc.contributor.authorRogaeva, Een_HK
dc.contributor.authorPremkumar, Sen_HK
dc.contributor.authorBrindle, Nen_HK
dc.contributor.authorKawarai, Ten_HK
dc.contributor.authorOrlacchio, Aen_HK
dc.contributor.authorYu, Gen_HK
dc.contributor.authorLevesque, Gen_HK
dc.contributor.authorNishimura, Men_HK
dc.contributor.authorIkeda, Men_HK
dc.contributor.authorPei, Yen_HK
dc.contributor.authorO'Toole, Cen_HK
dc.contributor.authorDuara, Ren_HK
dc.contributor.authorBarker, Wen_HK
dc.contributor.authorSorbi, Sen_HK
dc.contributor.authorFreedman, Men_HK
dc.contributor.authorFarrer, Len_HK
dc.contributor.authorSt GeorgeHyslop, Pen_HK
dc.date.accessioned2011-07-14T07:01:46Z-
dc.date.available2011-07-14T07:01:46Z-
dc.date.issued1998en_HK
dc.identifier.citationNeuroscience Letters, 1998, v. 250 n. 3, p. 189-192en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134744-
dc.description.abstractA novel polymorphism (-491 A/T) within the regulatory region on the apolipoprotein E gene has recently been reported to be associated with risk for Alzheimer disease (AD). To test this association in an independent data set, we have examined this polymorphism in a sample of 88 well-characterized AD cases and compared the allele frequency and genotype frequencies for this polymorphism with those observed in 112 cegnitively normal subjects drawn from the same ethnic group. These results suggest that in the current data set at least, the -491 NT polymorphism is not associated with risk for AD, but may be in partial linkage disequilibrium with the APOE ε2/ε3/ε4 polymorphism.en_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.subject-491 A/T polymorphismen_HK
dc.subjectAlzheimer diseaseen_HK
dc.subjectAPOE ε2/ε3/ε4 polymorphismen_HK
dc.subject.meshAgeden_US
dc.subject.meshAlzheimer Disease/*geneticsen_US
dc.subject.meshApolipoproteins E/*geneticsen_US
dc.subject.meshGene Frequencyen_US
dc.subject.meshHumansen_US
dc.subject.meshPolymorphism, Genetic/*geneticsen_US
dc.subject.meshRegulatory Sequences, Nucleic Acid/*geneticsen_US
dc.titleAbsence of association between Alzheimer disease and the -491 regulatory region polymorphism of APOEen_HK
dc.typeArticleen_HK
dc.identifier.emailSong, YQ:songy@hkucc.hku.hken_HK
dc.identifier.authoritySong, YQ=rp00488en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0304-3940(98)00470-4en_HK
dc.identifier.pmid9708864-
dc.identifier.scopuseid_2-s2.0-0032503943en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032503943&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume250en_HK
dc.identifier.issue3en_HK
dc.identifier.spage189en_HK
dc.identifier.epage192en_HK
dc.identifier.isiWOS:000075092500013-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridSong, YQ=7404921212en_HK
dc.identifier.scopusauthoridRogaeva, E=35372614800en_HK
dc.identifier.scopusauthoridPremkumar, S=6603080131en_HK
dc.identifier.scopusauthoridBrindle, N=7004637236en_HK
dc.identifier.scopusauthoridKawarai, T=34570127300en_HK
dc.identifier.scopusauthoridOrlacchio, A=35074779600en_HK
dc.identifier.scopusauthoridYu, G=36823639900en_HK
dc.identifier.scopusauthoridLevesque, G=7006678462en_HK
dc.identifier.scopusauthoridNishimura, M=15826903500en_HK
dc.identifier.scopusauthoridIkeda, M=7404692203en_HK
dc.identifier.scopusauthoridPei, Y=16741124100en_HK
dc.identifier.scopusauthoridO'Toole, C=7005035010en_HK
dc.identifier.scopusauthoridDuara, R=7005297173en_HK
dc.identifier.scopusauthoridBarker, W=8048862400en_HK
dc.identifier.scopusauthoridSorbi, S=7004417453en_HK
dc.identifier.scopusauthoridFreedman, M=7203068531en_HK
dc.identifier.scopusauthoridFarrer, L=7005139839en_HK
dc.identifier.scopusauthoridSt GeorgeHyslop, P=7005637468en_HK
dc.identifier.issnl0304-3940-

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