Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder

Ditte Demontis, Raymond K. Walters, Joanna Martin, Manuel Mattheisen, Thomas D. Als, Esben Agerbo, Gísli Baldursson, Rich Belliveau, Jonas Bybjerg‐Grauholm, Marie Bækvad‐Hansen, Felecia Cerrato, Kimberly Chambert, Claire Churchhouse, Ashley Dumont, Nicholas Eriksson, Michael J. Gandal, Jacqueline I. Goldstein, Katrina L. Grasby, Jakob Grove, Ólafur Ó. Guðmundsson, Christine Søholm Hansen, Mads E. Hauberg, Mads V. Hollegaard, Daniel P. Howrigan, Hailiang Huang, Julian Maller, Alicia R. Martin, Nicholas G. Martin, Jennifer L. Moran, Jonatan Pallesen, Duncan S. Palmer, Carsten Bøcker Pedersen, Marianne Giørtz Pedersen, Timothy Poterba, Jesper Buchhave Poulsen, Stephan Ripke, Elise Robinson, F. Kyle Satterstrom, Hreinn Stefánsson, Christine Stevens, Patrick Turley, G. Bragi Walters, Hyejung Won, Margaret J. Wright, Ole A. Andreassen, Philip Asherson, Christie L. Burton, Dorret I. Boomsma, Bru Cormand, Søren Dalsgaard, Barbara Franke, Joel Gelernter, Daniel H. Geschwind, Håkon Håkonarson, Jan Haavik, Henry R. Kranzler, Jonna Kuntsi, K. Langley, Klaus‐Peter Lesch, Christel M. Middeldorp, Andreas Reif, Luís Augusto Rohde, Panos Roussos, Russell Schachar, Pamela Sklar, Edmund Sonuga‐Barke, Patrick F. Sullivan, Anita Thapar, Joyce Y. Tung, Irwin D. Waldman, Sarah E. Medland, Kāri Stefánsson, Merete Nordentoft, David M. Hougaard, Thomas Werge, Ole Mors, Preben Bo Mortensen, Mark J. Daly, Stephen V. Faraone, Anders D. Børglum, Benjamin M. Neale

Nature Genetics · 2018

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Summary

Attention deficit/hyperactivity disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, finding important new information about the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes and around brain-expressed regulatory marks. Analyses of three replication studies: a cohort of individuals diagnosed with ADHD, a self-reported A

Source type: Peer-reviewed study
DOI: 10.1038/s41588-018-0269-7
Catalogue ID: SNmojad0uj-m2662v

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