Discovery Of The First Genome-Wide Significant Risk Loci For ADHD
By
Ditte Demontis,
Raymond K Walters,
Joanna Martin,
Manuel Mattheisen,
Thomas D. Als,
Esben Agerbo,
Rich Belliveau,
Jonas Bybjerg-Grauholm,
Marie Bækvad-Hansen,
Felecia Cerrato,
Kimberly Chambert,
Claire Churchhouse,
Ashley Dumont,
Nicholas Eriksson,
Michael Gandal,
Jacqueline Goldstein,
Jakob Grove,
Christine S. Hansen,
Mads E Hauberg,
Mads V Hollegaard,
Daniel P Howrigan,
Hailiang Huang,
Julian Maller,
Alicia R. Martin,
Jennifer Moran,
Jonatan Pallesen,
Duncan S. Palmer,
Carsten B Pedersen,
Marianne G Pedersen,
Timothy Poterba,
Jesper B Poulsen,
Stephan Ripke,
Elise B Robinson,
Kyle F Satterstrom,
Christine Stevens,
Patrick Turley,
Hyejung Won,
ADHD Working Group of the Psychiatric Genomics Consortium (PGC), Early Lifecourse & Genetic Epidemiology (EAGLE) Consortium, 23andMe Research Team,
Ole A. Andreassen,
Christie Burton,
Dorret Boomsma,
Bru Cormand,
Søren Dalsgaard,
Barbara Franke,
Joel Gelernter,
Daniel Geschwind,
Hakon Hakonarson,
Jan Haavik,
Henry Kranzler,
Jonna Kuntsi,
Kate Langley,
Klaus-Peter Lesch,
Christel Middeldorp,
Andreas Reif,
Luis A. Rohde,
Panos Roussos,
Russell Schachar,
Pamela Sklar,
Edmund Sonuga-Barke,
Patrick F Sullivan,
Anita Thapar,
Joyce Tung,
Irwin Waldman,
Merete Nordentoft,
David M Hougaard,
Thomas Werge,
Ole Mors,
Preben B Mortensen,
Mark J. Daly,
Stephen V. Faraone,
Anders D Børglum,
Benjamin M. Neale
Posted 03 Jun 2017
bioRxiv DOI: 10.1101/145581
(published DOI: 10.1038/s41588-018-0269-7)
Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of school-age children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no individual variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 ADHD cases and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, revealing new and important information on the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes, as well as around brain-expressed regulatory marks. These findings, based on clinical interviews and/or medical records are supported by additional analyses of a self-reported ADHD sample and a study of quantitative measures of ADHD symptoms in the population. Meta-analyzing these data with our primary scan yielded a total of 16 genome-wide significant loci. The results support the hypothesis that clinical diagnosis of ADHD is an extreme expression of one or more continuous heritable traits.
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