Case-control genome-wide association study of attention-deficit/hyperactivity disorder.
Case-control genome-wide association study of attention-deficit/hyperactivity disorder.
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DOI:
10.1016/j.jaac.2010.06.007
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发表时间:
2010-09
影响因子:
13.3
通讯作者:
IMAGE II Consortium Group
中科院分区:
文献类型:
--
作者:
Neale BM;Medland S;Ripke S;Anney RJ;Asherson P;Buitelaar J;Franke B;Gill M;Kent L;Holmans P;Middleton F;Thapar A;Lesch KP;Faraone SV;Daly M;Nguyen TT;Schäfer H;Steinhausen HC;Reif A;Renner TJ;Romanos M;Romanos J;Warnke A;Walitza S;Freitag C;Meyer J;Palmason H;Rothenberger A;Hawi Z;Sergeant J;Roeyers H;Mick E;Biederman J;IMAGE II Consortium Group
Although twin and family studies have shown attention deficit/hyperactivity disorder (ADHD) to be highly heritable, genetic variants influencing the trait at a genome-wide significant level have yet to be identified. Thus, additional genomewide association studies (GWAS) are needed. We used case-control analyses of 896 cases with DSM-IV ADHD genotyped using the Affymetrix 5.0 array and 2,455 repository controls screened for psychotic and bipolar symptoms genotyped using Affymetrix 6.0 arrays. A consensus SNP set was imputed using BEAGLE 3.0, resulting in an analysis dataset of 1,033,244 SNPs. The data were analyzed using a generalized linear model. No genome-wide significant associations were found. The most significant results implicated the following genes: PRKG1, FLNC, TCERG1L, PPM1H, NXPH1, PPM1H, CDH13, HK1 and HKDC1. The current analyses are a useful addition to the present literature and will make a valuable contribution to future meta-analyses. The candidate gene findings are consistent with a prior meta-analysis in suggesting that the effects of ADHD risk variants must, individually, be very small and/or include multiple rare alleles.
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影响因子:
11
作者:
Asherson, P.;Zhou, K.;Faraone, S. V.
通讯作者:
Faraone, S. V.
影响因子:
11
作者:
Brookes, K.;Xu, X.;Johansson, L.
通讯作者:
Johansson, L.
影响因子:
3
作者:
Faraone, Stephen V;Biederman, Joseph
通讯作者:
Biederman, Joseph
影响因子:
4.2
作者:
Faraone, Stephen V.;Adamson, Joel J.;Biederman, Joseph
通讯作者:
Biederman, Joseph
影响因子:
30.8
作者:
Ferreira, Manuel A. R.;O'Donovan, Michael C.;Meng, Yan A.;Jones, Ian R.;Ruderfer, Douglas M.;Jones, Lisa;Fan, Jinbo;Kirov, George;Perlis, Roy H.;Green, Elaine K.;Smoller, Jordan W.;Grozeva, Detelina;Stone, Jennifer;Nikolov, Ivan;Chambert, Kimberly;Hamshere, Marian L.;Nimgaonkar, Vishwajit L.;Moskvina, Valentina;Thase, Michael E.;Caesar, Sian;Sachs, Gary S.;Franklin, Jennifer;Gordon-Smith, Katherine;Ardlie, Kristin G.;Gabriel, Stacey B.;Fraser, Christine;Blumenstiel, Brendan;Defelice, Matthew;Breen, Gerome;Gill, Michael;Morris, Derek W.;Elkin, Amanda;Muir, Walter J.;McGhee, Kevin A.;Williamson, Richard;MacIntyre, Donald J.;MacLean, Alan W.;Clair, David St;Robinson, Michelle;Van Beck, Margaret;Pereira, Ana C. P.;Kandaswamy, Radhika;McQuillin, Andrew;Collier, David A.;Bass, Nicholas J.;Young, Allan H.;Lawrence, Jacob;Ferrier, I. Nicol;Anjorin, Adebayo;Farmer, Anne;Curtis, David;Scolnick, Edward M.;McGuffin, Peter;Daly, Mark J.;Corvin, Aiden P.;Holmans, Peter A.;Blackwood, Douglas H.;Gurling, Hugh M.;Owen, Michael J.;Purcell, Shaun M.;Sklar, Pamela;Craddock, Nick
通讯作者:
Craddock, Nick