Case-control genome-wide association study of attention-deficit/hyperactivity disorder

Neale, Benjamin M., Medland, Sarah, Ripke, Stephan, Anney, Richard ORCID: https://orcid.org/0000-0002-6083-407X, Asherson, Philip, Buitelaar, Jan, Franke, Barbara, Gill, Michael, Kent, Lindsey, Holmans, Peter Alan ORCID: https://orcid.org/0000-0003-0870-9412, Middleton, Frank, Thapar, Anita ORCID: https://orcid.org/0000-0002-3689-737X, Lesch, Klaus-Peter, Daly, Mark, Nguyen, Thuy Trang, Schäfer, Helmut, Steinhausen, Hans-Christoph, Reif, Andreas, Renner, Tobias J., Romanos, Marcel, Romanos, Jasmin, Warnke, Andreas, Walitza, Susanne, Freitag, Christine, Meyer, Jobst, Palmason, Haukur, Rothenberger, Aribert, Hawi, Ziarih, Sergeant, Joseph, Roeyers, Herbert, Mick, Eric and Biederman, Joseph 2010. Case-control genome-wide association study of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry 49 (9) , pp. 906-920. 10.1016/j.jaac.2010.06.007

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Abstract

Objective 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. Method 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. Data were analyzed using a generalized linear model. Results 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. Conclusions 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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI) MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG) Neuroscience and Mental Health Research Institute (NMHRI)
Subjects:	Q Science > QH Natural history > QH426 Genetics R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry R Medicine > RJ Pediatrics > RJ101 Child Health. Child health services
Uncontrolled Keywords:	ADHD, genetics, genome-wide association, imputation
Publisher:	Elsevier
ISSN:	0890-8567
Last Modified:	06 Dec 2022 09:42
URI:	https://orca.cardiff.ac.uk/id/eprint/25549

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