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Sökning: (WFRF:(Penninx BWJH)) pers:(Abdellaoui A) > Genetic effects inf...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005945naa a2201417 4500
001oai:prod.swepub.kib.ki.se:135537117
003SwePub
008240818s2017 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1355371172 URI
024a https://doi.org/10.1038/tp.2016.2922 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Bigdeli, TB4 aut
2451 0a Genetic effects influencing risk for major depressive disorder in China and Europe
264 c 2017-03-28
264 1b Springer Science and Business Media LLC,c 2017
520 a Major depressive disorder (MDD) is a common, complex psychiatric disorder and a leading cause of disability worldwide. Despite twin studies indicating its modest heritability (~30–40%), extensive heterogeneity and a complex genetic architecture have complicated efforts to detect associated genetic risk variants. We combined single-nucleotide polymorphism (SNP) summary statistics from the CONVERGE and PGC studies of MDD, representing 10 502 Chinese (5282 cases and 5220 controls) and 18 663 European (9447 cases and 9215 controls) subjects. We determined the fraction of SNPs displaying consistent directions of effect, assessed the significance of polygenic risk scores and estimated the genetic correlation of MDD across ancestries. Subsequent trans-ancestry meta-analyses combined SNP-level evidence of association. Sign tests and polygenic score profiling weakly support an overlap of SNP effects between East Asian and European populations. We estimated the trans-ancestry genetic correlation of lifetime MDD as 0.33; female-only and recurrent MDD yielded estimates of 0.40 and 0.41, respectively. Common variants downstream of GPHN achieved genome-wide significance by Bayesian trans-ancestry meta-analysis (rs9323497; log10 Bayes Factor=8.08) but failed to replicate in an independent European sample (P=0.911). Gene-set enrichment analyses indicate enrichment of genes involved in neuronal development and axonal trafficking. We successfully demonstrate a partially shared polygenic basis of MDD in East Asian and European populations. Taken together, these findings support a complex etiology for MDD and possible population differences in predisposing genetic factors, with important implications for future genetic studies.
700a Ripke, S4 aut
700a Peterson, RE4 aut
700a Trzaskowski, M4 aut
700a Bacanu, SA4 aut
700a Abdellaoui, A4 aut
700a Andlauer, TFM4 aut
700a Beekman, ATF4 aut
700a Berger, K4 aut
700a Blackwood, DHR4 aut
700a Boomsma, DI4 aut
700a Breen, G4 aut
700a Buttenschon, HN4 aut
700a Byrne, EM4 aut
700a Cichon, S4 aut
700a Clarke, TK4 aut
700a Couvy-Duchesne, B4 aut
700a Craddock, N4 aut
700a de Geus, EJC4 aut
700a Degenhardt, F4 aut
700a Dunn, EC4 aut
700a Edwards, AC4 aut
700a Fanous, AH4 aut
700a Forstner, AJ4 aut
700a Frank, J4 aut
700a Gill, M4 aut
700a Gordon, SD4 aut
700a Grabe, HJ4 aut
700a Hamilton, SP4 aut
700a Hardiman, O4 aut
700a Hayward, C4 aut
700a Heath, AC4 aut
700a Henders, AK4 aut
700a Herms, S4 aut
700a Hickie, IB4 aut
700a Hoffmann, P4 aut
700a Homuth, G4 aut
700a Hottenga, JJ4 aut
700a Ising, M4 aut
700a Jansen, R4 aut
700a Kloiber, S4 aut
700a Knowles, JA4 aut
700a Lang, M4 aut
700a Li, QS4 aut
700a Lucae, S4 aut
700a MacIntyre, DJ4 aut
700a Madden, PAF4 aut
700a Martin, NG4 aut
700a McGrath, PJ4 aut
700a McGuffin, P4 aut
700a McIntosh, AM4 aut
700a Medland, SE4 aut
700a Mehta, D4 aut
700a Middeldorp, CM4 aut
700a Milaneschi, Y4 aut
700a Montgomery, GW4 aut
700a Mors, O4 aut
700a Muller-Myhsok, B4 aut
700a Nauck, M4 aut
700a Nyholt, DR4 aut
700a Nothen, MM4 aut
700a Owen, MJ4 aut
700a Penninx, BWJH4 aut
700a Pergadia, ML4 aut
700a Perlis, RH4 aut
700a Peyrot, WJ4 aut
700a Porteous, DJ4 aut
700a Potash, JB4 aut
700a Rice, JP4 aut
700a Rietschel, M4 aut
700a Riley, BP4 aut
700a Rivera, M4 aut
700a Schoevers, R4 aut
700a Schulze, TG4 aut
700a Shi, J4 aut
700a Shyn, SI4 aut
700a Smit, JH4 aut
700a Smoller, JW4 aut
700a Streit, F4 aut
700a Strohmaier, J4 aut
700a Teumer, A4 aut
700a Treutlein, J4 aut
700a Van der Auwera, S4 aut
700a van Grootheest, G4 aut
700a van Hemert, AM4 aut
700a Volzke, H4 aut
700a Webb, BT4 aut
700a Weissman, MM4 aut
700a Wellmann, J4 aut
700a Willemsen, G4 aut
700a Witt, SH4 aut
700a Levinson, DF4 aut
700a Lewis, CM4 aut
700a Wray, NR4 aut
700a Flint, J4 aut
700a Sullivan, PFu Karolinska Institutet4 aut
700a Kendler, KS4 aut
710a Karolinska Institutet4 org
773t Translational psychiatryd : Springer Science and Business Media LLCg 7:3, s. e1074-q 7:3<e1074-x 2158-3188
856u https://www.nature.com/articles/tp2016292.pdf
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:135537117
8564 8u https://doi.org/10.1038/tp.2016.292

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