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FältnamnIndikatorerMetadata
00005780naa a2200901 4500
001oai:gup.ub.gu.se/262272
003SwePub
008240528s2017 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:137219589
024a https://gup.ub.gu.se/publication/2622722 URI
024a https://doi.org/10.1001/jamapsychiatry.2017.30692 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1372195892 URI
040 a (SwePub)gud (SwePub)ki
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Tielbeek, J. J.4 aut
2451 0a Genome-Wide Association Studies of a Broad Spectrum of Antisocial Behavior
264 1b American Medical Association (AMA),c 2017
520 a IMPORTANCE 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) (R-2 = 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.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Psykiatri0 (SwePub)302152 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Psychiatry0 (SwePub)302152 hsv//eng
653 a ld score regression
653 a early-childhood
653 a metaanalysis
653 a disorder
653 a heritability
653 a adolescence
653 a stability
653 a risk
653 a twin
653 a psychopathy
653 a Psychiatry
700a Johansson, Adau Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology4 aut
700a Polderman, T. J. C.u Karolinska Institutet4 aut
700a Rautiainen, M. R.4 aut
700a Jansen, P.4 aut
700a Taylor, M.4 aut
700a Tong, X.4 aut
700a Lu, Q.4 aut
700a Burt, A. S.4 aut
700a Tiemeier, H.4 aut
700a Viding, E.4 aut
700a Plomin, R.4 aut
700a Martin, N. G.4 aut
700a Heath, A. C.4 aut
700a Madden, P. A. F.4 aut
700a Montgomery, G.4 aut
700a Beaver, K. M.4 aut
700a Waldman, I.4 aut
700a Gelernter, J.4 aut
700a Kranzler, H. R.4 aut
700a Farrer, L. A.4 aut
700a Perry, J. R. B.4 aut
700a Munafo, M.4 aut
700a LoParo, D.4 aut
700a Paunio, T.4 aut
700a Tiihonen, J.4 aut
700a Mous, S. E.4 aut
700a Pappa, I.4 aut
700a de Leeuw, C.4 aut
700a Watanabe, K.4 aut
700a Hammerschlag, A. R.4 aut
700a Salvatore, J. E.4 aut
700a Aliev, F.4 aut
700a Bigdeli, T. B.4 aut
700a Dick, D.4 aut
700a Faraone, S. V.4 aut
700a Popma, A.4 aut
700a Medland, S. E.4 aut
700a Posthuma, D.4 aut
710a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi4 org
773t Jama Psychiatryd : American Medical Association (AMA)g 74:12, s. 1242-1250q 74:12<1242-1250x 2168-622Xx 2168-6238
856u https://jamanetwork.com/journals/jamapsychiatry/articlepdf/2656184/jamapsychiatry_tielbeek_2017_oi_170075.pdf
8564 8u https://gup.ub.gu.se/publication/262272
8564 8u https://doi.org/10.1001/jamapsychiatry.2017.3069
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:137219589

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