@article {Demontis145581, author = {Ditte Demontis and Raymond K. Walters and Joanna Martin and Manuel Mattheisen and Thomas D. Als and Esben Agerbo and Rich Belliveau and Jonas Bybjerg-Grauholm and Marie B{\ae}kvad-Hansen and Felecia Cerrato and Kimberly Chambert and Claire Churchhouse and Ashley Dumont and Nicholas Eriksson and Michael Gandal and Jacqueline Goldstein and Jakob Grove and Christine S. Hansen and Mads E. Hauberg and Mads V. Hollegaard and Daniel P. Howrigan and Hailiang Huang and Julian Maller and Alicia R. Martin and Jennifer Moran and Jonatan Pallesen and Duncan S. Palmer and Carsten B. Pedersen and Marianne G. Pedersen and Timothy Poterba and Jesper B. Poulsen and Stephan Ripke and Elise B. Robinson and Kyle F. Satterstrom and Christine Stevens and Patrick Turley and Hyejung Won and ADHD Working Group of the Psychiatric Genomics Consortium (PGC), Early Lifecourse \& Genetic Epidemiology (EAGLE) Consortium, 23andMe Research Team and Ole A. Andreassen and Christie Burton and Dorret Boomsma and Bru Cormand and S{\o}ren Dalsgaard and Barbara Franke and Joel Gelernter and Daniel Geschwind and Hakon Hakonarson and Jan Haavik and Henry Kranzler and Jonna Kuntsi and Kate Langley and Klaus-Peter Lesch and Christel Middeldorp and Andreas Reif and Luis A. Rohde and Panos Roussos and Russell Schachar and Pamela Sklar and Edmund Sonuga-Barke and Patrick F. Sullivan and Anita Thapar and Joyce Tung and Irwin Waldman and Merete Nordentoft and David M. Hougaard and Thomas Werge and Ole Mors and Preben B. Mortensen and Mark J. Daly and Stephen V. Faraone and Anders D. B{\o}rglum and Benjamin M. Neale}, title = {Discovery of the first genome-wide significant risk loci for ADHD}, elocation-id = {145581}, year = {2017}, doi = {10.1101/145581}, publisher = {Cold Spring Harbor Laboratory}, abstract = {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.}, URL = {https://www.biorxiv.org/content/early/2017/06/03/145581}, eprint = {https://www.biorxiv.org/content/early/2017/06/03/145581.full.pdf}, journal = {bioRxiv} }