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dc.date.accessioned2020-01-06T20:36:15Z
dc.date.available2020-01-06T20:36:15Z
dc.date.created2018-02-20T14:58:55Z
dc.date.issued2017
dc.identifier.citationShadrin, Alexey A. Smeland, Olav Bjerkehagen Zayats, Tetyana Schork, Andrew J Frei, Oleksandr Bettella, Francesco Witoelar, Aree Li, Wen Eriksen, Jon Alm Krull, Florian Djurovic, Srdjan Faraone, Stephen V. Reichborn-Kjennerud, Ted Thompson, Wesley K Johansson, Stefan Haavik, Jan Dale, Anders Wang, Yunpeng Andreassen, Ole Andreas . Novel loci associated with attention-deficit/hyperactivity disorder are revealed by leveraging polygenic overlap with educational attainment. Journal of the American Academy of Child and Adolescent Psychiatry. 2017, 57(2), 86-95
dc.identifier.urihttp://hdl.handle.net/10852/71913
dc.description.abstractObjective: Attention-deficit/hyperactivity disorder (ADHD) is a common and highly heritable psychiatric condition. By exploiting the reported relationship between ADHD and educational attainment (EA), we aimed to improve discovery of ADHD-associated genetic variants and to investigate genetic overlap between these phenotypes. Method: A conditional/conjunctional false discovery rate (condFDR/conjFDR) method was applied to genome-wide association study (GWAS) data on ADHD (2,064 trios, 896 cases, and 2,455 controls) and EA ( ) to identify ADHD-associated loci and loci overlapping between ADHD and EA. Identified single nucleotide polymorphisms (SNPs) were tested for association in an independent population-based study of ADHD symptoms (). Genetic correlation between ADHD and EA was estimated using LD score regression and Pearson correlation. Results: At levels of and we identified 5 ADHD-associated loci, 3 of these being shared between ADHD and EA. None of these loci had been identified in the primary ADHD GWAS, demonstrating the increased power provided by the condFDR/conjFDR analysis. Leading SNPs for 4 of 5 identified regions are in introns of protein coding genes (KDM4A, MEF2C, PINK1, RUNX1T1), whereas the remaining one is an intergenic SNP on chromosome 2 at 2p24. Consistent direction of effects in the independent study of ADHD symptoms was shown for 4 of 5 identified loci. A polygenic overlap between ADHD and EA was supported by significant genetic correlation (,) and >10-fold mutual enrichment of SNPs associated with both traits. Conclusion: We identified 5 novel loci associated with ADHD and provided evidence for a shared genetic basis between ADHD and EA. These findings could aid understanding of the genetic risk architecture of ADHD and its relation to EA.en_US
dc.languageEN
dc.publisherElsevier
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleNovel loci associated with attention-deficit/hyperactivity disorder are revealed by leveraging polygenic overlap with educational attainmenten_US
dc.typeJournal articleen_US
dc.creator.authorShadrin, Alexey A.
dc.creator.authorSmeland, Olav Bjerkehagen
dc.creator.authorZayats, Tetyana
dc.creator.authorSchork, Andrew J
dc.creator.authorFrei, Oleksandr
dc.creator.authorBettella, Francesco
dc.creator.authorWitoelar, Aree
dc.creator.authorLi, Wen
dc.creator.authorEriksen, Jon Alm
dc.creator.authorKrull, Florian
dc.creator.authorDjurovic, Srdjan
dc.creator.authorFaraone, Stephen V.
dc.creator.authorReichborn-Kjennerud, Ted
dc.creator.authorThompson, Wesley K
dc.creator.authorJohansson, Stefan
dc.creator.authorHaavik, Jan
dc.creator.authorDale, Anders
dc.creator.authorWang, Yunpeng
dc.creator.authorAndreassen, Ole Andreas
cristin.unitcode185,53,10,70
cristin.unitnameNORMENT part UiO
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode2
dc.identifier.cristin1567090
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Journal of the American Academy of Child and Adolescent Psychiatry&rft.volume=57&rft.spage=86&rft.date=2017
dc.identifier.jtitleJournal of the American Academy of Child and Adolescent Psychiatry
dc.identifier.volume57
dc.identifier.issue2
dc.identifier.startpage86
dc.identifier.endpage95
dc.identifier.doihttps://doi.org/10.1016/j.jaac.2017.11.013
dc.identifier.urnURN:NBN:no-75036
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn0890-8567
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/71913/1/Shadrin_ADHD_EA.pdf
dc.type.versionAcceptedVersion
dc.relation.projectNFR/248778
dc.relation.projectNFR/248980
dc.relation.projectNFR/223273
dc.relation.projectNFR/251134
dc.relation.projectEU/667302
dc.relation.projectNFR/213694


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