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dc.contributor.authorADHD Working Group of the Psychiatric Genomics Consortium (PGC)
dc.contributor.authorEarly Lifecourse & Genetic Epidemiology (EAGLE) Consortium
dc.contributor.author23andMe Research Team
dc.contributor.authorKent, Lindsey
dc.date.accessioned2020-10-27T16:56:41Z
dc.date.available2020-10-27T16:56:41Z
dc.date.issued2019-01
dc.identifier.citationADHD Working Group of the Psychiatric Genomics Consortium (PGC) , Early Lifecourse & Genetic Epidemiology (EAGLE) Consortium , 23andMe Research Team & Kent , L 2019 , ' Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder ' , Nature Genetics , vol. 51 , no. 1 , pp. 63-75 . https://doi.org/10.1038/s41588-018-0269-7en
dc.identifier.issn1061-4036
dc.identifier.otherPURE: 270391608
dc.identifier.otherPURE UUID: 59ecb314-b4e4-451b-b114-41cbe0f61ec3
dc.identifier.otherPubMed: 30478444
dc.identifier.otherPubMedCentral: PMC6481311
dc.identifier.otherScopus: 85057436335
dc.identifier.otherORCID: /0000-0002-5315-3399/work/81405655
dc.identifier.otherWOS: 000454108800014
dc.identifier.urihttps://hdl.handle.net/10023/20827
dc.description.abstractAttention deficit/hyperactivity disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, finding important new information about the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes and around brain-expressed regulatory marks. Analyses of three replication studies: a cohort of individuals diagnosed with ADHD, a self-reported ADHD sample and a meta-analysis of quantitative measures of ADHD symptoms in the population, support these findings while highlighting study-specific differences on genetic overlap with educational attainment. Strong concordance with GWAS of quantitative population measures of ADHD symptoms supports that clinical diagnosis of ADHD is an extreme expression of continuous heritable traits.
dc.format.extent13
dc.language.isoeng
dc.relation.ispartofNature Geneticsen
dc.rightsCopyright © 2020 the Author(s). This work has been made available online in accordance with publisher policies or with permission. Permission for further reuse of this content should be sought from the publisher or the rights holder. This is the author created accepted manuscript following peer review and may differ slightly from the final published version. The final published version of this work is available at https://doi.org/10.1038/s41588-018-0269-7.en
dc.subjectAdolescenten
dc.subjectAttention Deficit Disorder with Hyperactivity/geneticsen
dc.subjectBrain/physiologyen
dc.subjectChilden
dc.subjectChild, Preschoolen
dc.subjectCohort Studiesen
dc.subjectFemaleen
dc.subjectGene Expression Regulation/geneticsen
dc.subjectGenetic Loci/geneticsen
dc.subjectGenetic Predisposition to Disease/geneticsen
dc.subjectGenome-Wide Association Study/methodsen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectPolymorphism, Single Nucleotide/geneticsen
dc.subjectRisken
dc.subjectQH426 Geneticsen
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.subject3rd-DASen
dc.subject.lccQH426en
dc.subject.lccRC0321en
dc.titleDiscovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorderen
dc.typeJournal articleen
dc.description.versionPostprinten
dc.contributor.institutionUniversity of St Andrews. Cellular Medicine Divisionen
dc.contributor.institutionUniversity of St Andrews. Institute of Behavioural and Neural Sciencesen
dc.contributor.institutionUniversity of St Andrews. School of Medicineen
dc.identifier.doihttps://doi.org/10.1038/s41588-018-0269-7
dc.description.statusPeer revieweden
dc.date.embargoedUntil2019-05-26
dc.identifier.urlhttp://orca.cf.ac.uk/id/eprint/110923en


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