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dc.contributor.authorMartin, Joanna
dc.contributor.authorWalters, Raymond K.
dc.contributor.authorDemontis, Ditte
dc.contributor.authorMattheisen, Manuel
dc.contributor.authorHong Lee, S.
dc.contributor.authorRobinson, Elise
dc.contributor.authorBrikell, Isabell
dc.contributor.authorGhirardi, Laura
dc.contributor.authorLarsson, Henrik
dc.contributor.authorLichtenstein, Paul
dc.contributor.authorEriksson, Nicholas
dc.contributor.author23andMe Research Team
dc.contributor.authorPsychiatric Genomics Consortium: ADHD Subgroup
dc.contributor.authoriPSYCH–Broad ADHD Workgroup
dc.contributor.authorWerge, Thomas
dc.contributor.authorMortensen, Preben Bo
dc.contributor.authorPedersen, Marianne Giørtz
dc.contributor.authorMors, Ole
dc.contributor.authorNordentoft, Merete
dc.contributor.authorHougaard, David M.
dc.contributor.authorBybjerg-Grauholm, Jonas
dc.contributor.authorWray, Naomi R.
dc.contributor.authorFranke, Barbara
dc.contributor.authorFaraone, Stephen V.
dc.contributor.authorO'Donovan, Michael C.
dc.contributor.authorThapar, Anita
dc.contributor.authorBørglum, Anders D.
dc.contributor.authorNeale, Benjamin M.
dc.contributor.authorKent, Lindsey
dc.identifier.citationMartin , J , Walters , R K , Demontis , D , Mattheisen , M , Hong Lee , S , Robinson , E , Brikell , I , Ghirardi , L , Larsson , H , Lichtenstein , P , Eriksson , N , 23andMe Research Team , Psychiatric Genomics Consortium: ADHD Subgroup , iPSYCH–Broad ADHD Workgroup , Werge , T , Mortensen , P B , Pedersen , M G , Mors , O , Nordentoft , M , Hougaard , D M , Bybjerg-Grauholm , J , Wray , N R , Franke , B , Faraone , S V , O'Donovan , M C , Thapar , A , Børglum , A D , Neale , B M & Kent , L 2018 , ' A genetic investigation of sex bias in the prevalence of attention-deficit/hyperactivity disorder ' , Biological Psychiatry , vol. 83 , no. 12 , pp. 1044-1053 .
dc.identifier.otherORCID: /0000-0002-5315-3399/work/81405654
dc.descriptionThis work was supported by the National Human Genome Research Institute of the National Institutes of Health (NIH) (Grant No. R44HG006981 to the 23andMe Team), the Wellcome Trust (Grant No. 106047 to JM). the Australian National Health and Medical Research Council (Grant Nos. 1078901 and 1087889 to NRW). The Broad Institute and Massachusetts General Hospital investigators acknowledge support from the Stanley Medical Research Institute and NIH grants: Grant No. 1R01MH094469 (principal investigator, BMN) and Grant No. 1R01MH107649-01 (principal investigator, BMN). The iPSYCH team acknowledges funding from the Lundbeck Foundation (Grant Nos. R102-A9118 and R155-2014-1724), the Stanley Medical Research Institute, the European Research Council (Project No. 294838), the European Community’s Horizon 2020 Programme (H2020/2014-2020) under Grant No. 667302 (Comorbid Conditions of ADHD), the Novo Nordisk Foundation for supporting the Danish National Biobank resource, and grants from Aarhus and Copenhagen universities and university hospitals, including support to the Centre for Integrative Sequencing, the GenomeDK HPC facility, and the Centre for Integrated Register-Based Research at Aarhus University.en
dc.description.abstractBackground Attention-deficit/hyperactivity disorder (ADHD) shows substantial heritability and is two to seven times more common in male individuals than in female individuals. We examined two putative genetic mechanisms underlying this sex bias: sex-specific heterogeneity and higher burden of risk in female cases. Methods We analyzed genome-wide autosomal common variants from the Psychiatric Genomics Consortium and iPSYCH Project (n = 20,183 cases, n = 35,191 controls) and Swedish population register data (n = 77,905 cases, n = 1,874,637 population controls). Results Genetic correlation analyses using two methods suggested near complete sharing of common variant effects across sexes, with rg estimates close to 1. Analyses of population data, however, indicated that female individuals with ADHD may be at especially high risk for certain comorbid developmental conditions (i.e., autism spectrum disorder and congenital malformations), potentially indicating some clinical and etiological heterogeneity. Polygenic risk score analysis did not support a higher burden of ADHD common risk variants in female cases (odds ratio [confidence interval] = 1.02 [0.98–1.06], p = .28). In contrast, epidemiological sibling analyses revealed that the siblings of female individuals with ADHD are at higher familial risk for ADHD than the siblings of affected male individuals (odds ratio [confidence interval] = 1.14 [1.11–1.18], p = 1.5E-15). Conclusions Overall, this study supports a greater familial burden of risk in female individuals with ADHD and some clinical and etiological heterogeneity, based on epidemiological analyses. However, molecular genetic analyses suggest that autosomal common variants largely do not explain the sex bias in ADHD prevalence.
dc.relation.ispartofBiological Psychiatryen
dc.subjectNeurodevelopmental disordersen
dc.subjectPolygenic risk score analysisen
dc.subjectSex biasen
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.subjectBiological Psychiatryen
dc.titleA genetic investigation of sex bias in the prevalence of attention-deficit/hyperactivity disorderen
dc.typeJournal articleen
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.description.statusPeer revieweden

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