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dc.contributor.authorTielbeek, Jorim J
dc.contributor.authorJohansson, Ada
dc.contributor.authorPolderman, Tinca JC
dc.contributor.authorRautiainen, Marja-Riitta
dc.contributor.authorJansen, Philip
dc.contributor.authorTaylor, Michelle
dc.contributor.authorTong, Xiaoran
dc.contributor.authorLu, Qing
dc.contributor.authorBurt, Alexandra S
dc.contributor.authorTiemeier, Henning
dc.contributor.authorViding, Essi
dc.contributor.authorPlomin, Robert
dc.contributor.authorMartin, Nicholas G
dc.contributor.authorHeath, Andrew C
dc.contributor.authorMadden, Pamela AF
dc.contributor.authorMontgomery, Grant
dc.contributor.authorBeaver, Kevin M
dc.contributor.authorWaldman, Irwin
dc.contributor.authorGelernter, Joel
dc.contributor.authorKranzler, Henry R
dc.contributor.authorFarrer, Lindsay A
dc.contributor.authorPerry, John
dc.contributor.authorMunafò, Marcus
dc.contributor.authorLoParo, Devon
dc.contributor.authorPaunio, Tiina
dc.contributor.authorTiihonen, Jari
dc.contributor.authorMous, Sabine E
dc.contributor.authorPappa, Irene
dc.contributor.authorde Leeuw, Christiaan
dc.contributor.authorWatanabe, Kyoko
dc.contributor.authorHammerschlag, Anke R
dc.contributor.authorSalvatore, Jessica E
dc.contributor.authorAliev, Fazil
dc.contributor.authorBigdeli, Tim B
dc.contributor.authorDick, Danielle
dc.contributor.authorFaraone, Stephen V
dc.contributor.authorPopma, Arne
dc.contributor.authorMedland, Sarah E
dc.contributor.authorPosthuma, Danielle
dc.contributor.authorBroad Antisocial Behavior Consortium collaborators
dc.date.accessioned2018-11-22T00:30:09Z
dc.date.available2018-11-22T00:30:09Z
dc.date.issued2017-12-01
dc.identifier.issn2168-622X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/285573
dc.description.abstractImportance: Antisocial behavior (ASB) places a large burden on perpetrators, survivors, and society. Twin studies indicate that half of the variation in this trait is genetic. Specific causal genetic variants have, however, not been identified. Objectives: To estimate the single-nucleotide polymorphism-based heritability of ASB; to identify novel genetic risk variants, genes, or biological pathways; to test for pleiotropic associations with other psychiatric traits; and to reevaluate the candidate gene era data through the Broad Antisocial Behavior Consortium. Design, Setting, and Participants: Genome-wide association data from 5 large population-based cohorts and 3 target samples with genome-wide genotype and ASB data were used for meta-analysis from March 1, 2014, to May 1, 2016. All data sets used quantitative phenotypes, except for the Finnish Crime Study, which applied a case-control design (370 patients and 5850 control individuals). Main Outcome and Measures: This study adopted relatively broad inclusion criteria to achieve a quantitative measure of ASB derived from multiple measures, maximizing the sample size over different age ranges. Results: The discovery samples comprised 16 400 individuals, whereas the target samples consisted of 9381 individuals (all individuals were of European descent), including child and adult samples (mean age range, 6.7-56.1 years). Three promising loci with sex-discordant associations were found (8535 female individuals, chromosome 1: rs2764450, chromosome 11: rs11215217; 7772 male individuals, chromosome X, rs41456347). Polygenic risk score analyses showed prognostication of antisocial phenotypes in an independent Finnish Crime Study (2536 male individuals and 3684 female individuals) and shared genetic origin with conduct problems in a population-based sample (394 male individuals and 431 female individuals) but not with conduct disorder in a substance-dependent sample (950 male individuals and 1386 female individuals) (R2 = 0.0017 in the most optimal model, P = 0.03). Significant inverse genetic correlation of ASB with educational attainment (r = -0.52, P = .005) was detected. Conclusions and Relevance: The Broad Antisocial Behavior Consortium entails the largest collaboration to date on the genetic architecture of ASB, and the first results suggest that ASB may be highly polygenic and has potential heterogeneous genetic effects across sex.
dc.format.mediumPrint
dc.languageeng
dc.publisherAmerican Medical Association (AMA)
dc.subjectBroad Antisocial Behavior Consortium collaborators
dc.subjectHumans
dc.subjectConduct Disorder
dc.subjectAntisocial Personality Disorder
dc.subjectEnvironment
dc.subjectSex Factors
dc.subjectMultifactorial Inheritance
dc.subjectAdolescent
dc.subjectAdult
dc.subjectMiddle Aged
dc.subjectChild
dc.subjectFinland
dc.subjectFemale
dc.subjectMale
dc.subjectGenetic Variation
dc.subjectGenome-Wide Association Study
dc.titleGenome-Wide Association Studies of a Broad Spectrum of Antisocial Behavior.
dc.typeArticle
prism.endingPage1250
prism.issueIdentifier12
prism.publicationDate2017
prism.publicationNameJAMA Psychiatry
prism.startingPage1242
prism.volume74
dc.identifier.doi10.17863/CAM.32928
dcterms.dateAccepted2017-08-03
rioxxterms.versionofrecord10.1001/jamapsychiatry.2017.3069
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2017-12
dc.contributor.orcidPerry, John [0000-0001-6483-3771]
dc.identifier.eissn2168-6238
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MC_UU_12015/2)
rioxxterms.freetoread.startdate2018-12-31


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