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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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