File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Quantitative trait locus analysis of candidate gene alleles associated with attention deficit hyperactivity disorder (ADHD) in five genes: DRD4, DAT1, DRD5, SNAP-25, and 5HT1B

TitleQuantitative trait locus analysis of candidate gene alleles associated with attention deficit hyperactivity disorder (ADHD) in five genes: DRD4, DAT1, DRD5, SNAP-25, and 5HT1B
Authors
Keywords5HT1B
Association
Attention-deficit hyperactivity disorder (ADHD)
DAT1
DRD4
DRD5
Genetics
Quantitative trait loci (QTL)
Quantitative-TDT (Q-TDT)
SNAP-25
Issue Date2005
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, 2005, v. 133 B n. 1, p. 68-73 How to Cite?
AbstractIt has been widely postulated that the categorical diagnosis of attention deficit hyperactivity disorder (ADHD) should be seen as the extreme end of a set of traits quantitatively distributed in the general population. A consequence of this is that the genes associated with DSM-IV ADHD should also influence these underlying traits in non-affected individuals. The aim of this study was to examine if specific candidate loci previously shown to be associated with DSM-IV ADHD, also act as quantitative trait loci (QTLs) for ADHD-symptoms in the general population. We have genotyped five candidate markers in a population-based sample of male dizygous twin-pairs (n = 329 pairs). We found little evidence to support a role for the previously-nominated alleles of a DRD4 VNTR, a 5HT1B SNP, or a microsatellite marker near to DRD5, in the distribution of ADHD-symptoms scores; however, we found some evidence to suggest that the DAT1 3′UTR VNTR and weak evidence that a microsatellite in SNAP-25 may have a role in continuous measures of ADHD-symptoms hyperactivity above and beyond their role in clinical ADHD. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/175912
ISSN
2021 Impact Factor: 3.358
2020 SCImago Journal Rankings: 1.393
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMill, Jen_US
dc.contributor.authorXu, Xen_US
dc.contributor.authorRonald, Aen_US
dc.contributor.authorCurran, Sen_US
dc.contributor.authorPrice, Ten_US
dc.contributor.authorKnight, Jen_US
dc.contributor.authorCraig, Ien_US
dc.contributor.authorSham, Pen_US
dc.contributor.authorPlomin, Ren_US
dc.contributor.authorAsherson, Pen_US
dc.date.accessioned2012-11-26T09:02:25Z-
dc.date.available2012-11-26T09:02:25Z-
dc.date.issued2005en_US
dc.identifier.citationAmerican Journal Of Medical Genetics - Neuropsychiatric Genetics, 2005, v. 133 B n. 1, p. 68-73en_US
dc.identifier.issn1552-4841en_US
dc.identifier.urihttp://hdl.handle.net/10722/175912-
dc.description.abstractIt has been widely postulated that the categorical diagnosis of attention deficit hyperactivity disorder (ADHD) should be seen as the extreme end of a set of traits quantitatively distributed in the general population. A consequence of this is that the genes associated with DSM-IV ADHD should also influence these underlying traits in non-affected individuals. The aim of this study was to examine if specific candidate loci previously shown to be associated with DSM-IV ADHD, also act as quantitative trait loci (QTLs) for ADHD-symptoms in the general population. We have genotyped five candidate markers in a population-based sample of male dizygous twin-pairs (n = 329 pairs). We found little evidence to support a role for the previously-nominated alleles of a DRD4 VNTR, a 5HT1B SNP, or a microsatellite marker near to DRD5, in the distribution of ADHD-symptoms scores; however, we found some evidence to suggest that the DAT1 3′UTR VNTR and weak evidence that a microsatellite in SNAP-25 may have a role in continuous measures of ADHD-symptoms hyperactivity above and beyond their role in clinical ADHD. © 2005 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.subject5HT1B-
dc.subjectAssociation-
dc.subjectAttention-deficit hyperactivity disorder (ADHD)-
dc.subjectDAT1-
dc.subjectDRD4-
dc.subjectDRD5-
dc.subjectGenetics-
dc.subjectQuantitative trait loci (QTL)-
dc.subjectQuantitative-TDT (Q-TDT)-
dc.subjectSNAP-25-
dc.subject.meshAllelesen_US
dc.subject.meshAttention Deficit Disorder With Hyperactivity - Geneticsen_US
dc.subject.meshChilden_US
dc.subject.meshDopamine Plasma Membrane Transport Proteinsen_US
dc.subject.meshGene Frequencyen_US
dc.subject.meshGenetic Predisposition To Disease - Geneticsen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshLinkage Disequilibriumen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Glycoproteins - Geneticsen_US
dc.subject.meshMembrane Proteins - Geneticsen_US
dc.subject.meshMembrane Transport Proteins - Geneticsen_US
dc.subject.meshMeta-Analysis As Topicen_US
dc.subject.meshNerve Tissue Proteins - Geneticsen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshQuantitative Trait Loci - Geneticsen_US
dc.subject.meshReceptor, Serotonin, 5-Ht1b - Geneticsen_US
dc.subject.meshReceptors, Dopamine D1 - Geneticsen_US
dc.subject.meshReceptors, Dopamine D2 - Geneticsen_US
dc.subject.meshReceptors, Dopamine D4en_US
dc.subject.meshReceptors, Dopamine D5en_US
dc.subject.meshSynaptosomal-Associated Protein 25en_US
dc.subject.meshTwins, Dizygotic - Geneticsen_US
dc.titleQuantitative trait locus analysis of candidate gene alleles associated with attention deficit hyperactivity disorder (ADHD) in five genes: DRD4, DAT1, DRD5, SNAP-25, and 5HT1Ben_US
dc.typeArticleen_US
dc.identifier.emailSham, P: pcsham@hku.hken_US
dc.identifier.authoritySham, P=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/ajmg.b.30107en_US
dc.identifier.pmid15578613-
dc.identifier.scopuseid_2-s2.0-15744363362en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-15744363362&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume133 Ben_US
dc.identifier.issue1en_US
dc.identifier.spage68en_US
dc.identifier.epage73en_US
dc.identifier.isiWOS:000226619600013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMill, J=7006450209en_US
dc.identifier.scopusauthoridXu, X=7405294989en_US
dc.identifier.scopusauthoridRonald, A=8274862900en_US
dc.identifier.scopusauthoridCurran, S=7103220956en_US
dc.identifier.scopusauthoridPrice, T=7202062065en_US
dc.identifier.scopusauthoridKnight, J=13002769800en_US
dc.identifier.scopusauthoridCraig, I=7102548208en_US
dc.identifier.scopusauthoridSham, P=34573429300en_US
dc.identifier.scopusauthoridPlomin, R=36050187200en_US
dc.identifier.scopusauthoridAsherson, P=35402700900en_US
dc.identifier.issnl1552-4841-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats