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Article: Linkage Disequilibrium Analysis of Polymorphisms in the Gene for Myelin Oligodendrocyte Glycoprotein in Tourette's Syndrome Patients from a Chinese Sample

TitleLinkage Disequilibrium Analysis of Polymorphisms in the Gene for Myelin Oligodendrocyte Glycoprotein in Tourette's Syndrome Patients from a Chinese Sample
Authors
Issue Date2004
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0148-7299:1/
Citation
American Journal Of Medical Genetics - Neuropsychiatric Genetics, 2004, v. 124 B n. 1, p. 76-80 How to Cite?
AbstractGilles de la Tourette syndrome (GTS) is a neuropsychiatric disorder characterised by multiple motor and phonic tics, which wax and wane. Recently, evidence has accumulated supporting the role of autoimmune mechanisms in the aetiology of GTS, suggesting that it is within the paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) spectrum of childhood neurobehavioural disorders. An immunopathogenic role of antibodies against myelin oligodendrocyte glycoprotein (MOG) has been suggested in this syndrome. In this study, we investigate the association of three microsatellite polymorphisms (MOGa, MOGb, MOGc) in the gene for MOG with GTS in 197 family trios collected from southwest China. Linkage disequilibrium between these three markers was observed with the strongest between MOGa and MOGc (D′=0.541, P = 0.000). We did not find overall significant evidence for distorted transmission of any of these three markers of MOG gene in GTS, although we observed a weak preferential transmission of the 148 bp allele of MOGc (χ2 = 4.000, P = 0.046) which did not survive correction for multiple testing. Our results suggest that there is no association between the MOG gene polymorphisms we tested and GTS. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/175897
ISSN
2015 Impact Factor: 3.391
2015 SCImago Journal Rankings: 1.771
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuang, Yen_US
dc.contributor.authorLi, Ten_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorAnsar, Jen_US
dc.contributor.authorLanting, Gen_US
dc.contributor.authorLiu, Xen_US
dc.contributor.authorZhao, JHen_US
dc.contributor.authorHu, Xen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorCollier, Den_US
dc.date.accessioned2012-11-26T09:02:16Z-
dc.date.available2012-11-26T09:02:16Z-
dc.date.issued2004en_US
dc.identifier.citationAmerican Journal Of Medical Genetics - Neuropsychiatric Genetics, 2004, v. 124 B n. 1, p. 76-80en_US
dc.identifier.issn1552-4841en_US
dc.identifier.urihttp://hdl.handle.net/10722/175897-
dc.description.abstractGilles de la Tourette syndrome (GTS) is a neuropsychiatric disorder characterised by multiple motor and phonic tics, which wax and wane. Recently, evidence has accumulated supporting the role of autoimmune mechanisms in the aetiology of GTS, suggesting that it is within the paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) spectrum of childhood neurobehavioural disorders. An immunopathogenic role of antibodies against myelin oligodendrocyte glycoprotein (MOG) has been suggested in this syndrome. In this study, we investigate the association of three microsatellite polymorphisms (MOGa, MOGb, MOGc) in the gene for MOG with GTS in 197 family trios collected from southwest China. Linkage disequilibrium between these three markers was observed with the strongest between MOGa and MOGc (D′=0.541, P = 0.000). We did not find overall significant evidence for distorted transmission of any of these three markers of MOG gene in GTS, although we observed a weak preferential transmission of the 148 bp allele of MOGc (χ2 = 4.000, P = 0.046) which did not survive correction for multiple testing. Our results suggest that there is no association between the MOG gene polymorphisms we tested and GTS. © 2003 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0148-7299:1/en_US
dc.relation.ispartofAmerican Journal of Medical Genetics - Neuropsychiatric Geneticsen_US
dc.subject.meshChinaen_US
dc.subject.meshDna - Chemistry - Geneticsen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshLinkage Disequilibriumen_US
dc.subject.meshMaleen_US
dc.subject.meshMicrosatellite Repeatsen_US
dc.subject.meshMyelin Proteinsen_US
dc.subject.meshMyelin-Associated Glycoprotein - Geneticsen_US
dc.subject.meshNuclear Familyen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshTourette Syndrome - Genetics - Pathologyen_US
dc.titleLinkage Disequilibrium Analysis of Polymorphisms in the Gene for Myelin Oligodendrocyte Glycoprotein in Tourette's Syndrome Patients from a Chinese Sampleen_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.doi10.1002/ajmg.b.20079-
dc.identifier.pmid14681920-
dc.identifier.scopuseid_2-s2.0-0347363528en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0347363528&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume124 Ben_US
dc.identifier.issue1en_US
dc.identifier.spage76en_US
dc.identifier.epage80en_US
dc.identifier.isiWOS:000189186100017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHuang, Y=35596180300en_US
dc.identifier.scopusauthoridLi, T=36072008200en_US
dc.identifier.scopusauthoridWang, Y=7601489039en_US
dc.identifier.scopusauthoridAnsar, J=13203889100en_US
dc.identifier.scopusauthoridLanting, G=6504183503en_US
dc.identifier.scopusauthoridLiu, X=7409286408en_US
dc.identifier.scopusauthoridZhao, JH=7410311266en_US
dc.identifier.scopusauthoridHu, X=7404709241en_US
dc.identifier.scopusauthoridSham, PC=34573429300en_US
dc.identifier.scopusauthoridCollier, D=26642980600en_US

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