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Article: Chromosome 22 markers demonstrate transmission disequilibrium with schizophrenia

TitleChromosome 22 markers demonstrate transmission disequilibrium with schizophrenia
Authors
KeywordsChromosome 22
Schizophrenia
Issue Date1995
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.psychgenetics.com
Citation
Psychiatric Genetics, 1995, v. 5 n. 3, p. 127-130 How to Cite?
AbstractPreviously we reported evidence for genetic linkage between markers on chromosome 22q12 and schizophrenia in 23 multiply affected pedigrees. As part of further investigation of this region, we have applied the transmission disequilibrium test (TDT) to the genotype data. The TDT is a test for both linkage and linkage disequilibrium, and is based on the unequal probability of transmission of two different marker alleles from parents to affected offspring. We obtained significant results for the marker D22S283 (χ 2 35.9, 14 df, p = 0.001), D22S278 (χ 2 = 16.5, 6 df, p = 0.01) and F8VWFP (χ 2 = 13.1, 4 df, P = 0.01) Application of the Bonferonni correction for testing multiple markers renders the results for marker D22S278 and F8VWFP non-significant (from p = 0.01 to p = 0.14), while the result for D22S283 remains modestly significant at p < 0.02. Overall, our findings strengthen the suggestion that the region around D22S283 contains a susceptibility gene for schizophrenia.
Persistent Identifierhttp://hdl.handle.net/10722/175738
ISSN
2023 Impact Factor: 1.5
2023 SCImago Journal Rankings: 0.629
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVallada, Hen_US
dc.contributor.authorCurtis, Den_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorMurray, RMen_US
dc.contributor.authorMcguffin, Pen_US
dc.contributor.authorNanko, Sen_US
dc.contributor.authorGill, Men_US
dc.contributor.authorOwen, Men_US
dc.contributor.authorCollier, DAen_US
dc.date.accessioned2012-11-26T09:00:52Z-
dc.date.available2012-11-26T09:00:52Z-
dc.date.issued1995en_US
dc.identifier.citationPsychiatric Genetics, 1995, v. 5 n. 3, p. 127-130en_US
dc.identifier.issn0955-8829en_US
dc.identifier.urihttp://hdl.handle.net/10722/175738-
dc.description.abstractPreviously we reported evidence for genetic linkage between markers on chromosome 22q12 and schizophrenia in 23 multiply affected pedigrees. As part of further investigation of this region, we have applied the transmission disequilibrium test (TDT) to the genotype data. The TDT is a test for both linkage and linkage disequilibrium, and is based on the unequal probability of transmission of two different marker alleles from parents to affected offspring. We obtained significant results for the marker D22S283 (χ 2 35.9, 14 df, p = 0.001), D22S278 (χ 2 = 16.5, 6 df, p = 0.01) and F8VWFP (χ 2 = 13.1, 4 df, P = 0.01) Application of the Bonferonni correction for testing multiple markers renders the results for marker D22S278 and F8VWFP non-significant (from p = 0.01 to p = 0.14), while the result for D22S283 remains modestly significant at p < 0.02. Overall, our findings strengthen the suggestion that the region around D22S283 contains a susceptibility gene for schizophrenia.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.psychgenetics.comen_US
dc.relation.ispartofPsychiatric Geneticsen_US
dc.subjectChromosome 22-
dc.subjectSchizophrenia-
dc.subject.meshChromosome Mappingen_US
dc.subject.meshChromosomes, Human, Pair 22en_US
dc.subject.meshFemaleen_US
dc.subject.meshGenetic Linkageen_US
dc.subject.meshGenetic Markersen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshLinkage Disequilibriumen_US
dc.subject.meshMaleen_US
dc.subject.meshPedigreeen_US
dc.subject.meshProbabilityen_US
dc.subject.meshSchizophrenia - Geneticsen_US
dc.titleChromosome 22 markers demonstrate transmission disequilibrium with schizophreniaen_US
dc.typeArticleen_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00041444-199505030-00005-
dc.identifier.pmid8746411-
dc.identifier.scopuseid_2-s2.0-0029561772en_US
dc.identifier.volume5en_US
dc.identifier.issue3en_US
dc.identifier.spage127en_US
dc.identifier.epage130en_US
dc.identifier.isiWOS:A1995TN62800005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVallada, H=7003742958en_US
dc.identifier.scopusauthoridCurtis, D=14633020700en_US
dc.identifier.scopusauthoridSham, PC=34573429300en_US
dc.identifier.scopusauthoridMurray, RM=35406239400en_US
dc.identifier.scopusauthoridMcGuffin, P=22954119700en_US
dc.identifier.scopusauthoridNanko, S=7006294283en_US
dc.identifier.scopusauthoridGill, M=14633481100en_US
dc.identifier.scopusauthoridOwen, M=36044041500en_US
dc.identifier.scopusauthoridCollier, DA=26642980600en_US
dc.identifier.issnl0955-8829-

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