About this item:

87 Views | 24 Downloads

Author Notes:

See publication for full list of authors.

Correspond with: Benjamin M. Neale (bneale@broadinstitute.org), Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. Anders D. Børglum (anders@biomed.au.dk) Department of Biomedicine - Human Genetics, Aarhus University, Aarhus, Denmark. Stephen V. Faraone(sfaraone@childpsychresearch.org) Departments of Psychiatry and Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, New York, USA.

See publication for full list of author contributions.

We thank T., Lehner, A. Addington and G. Senthil for their support in the Psychiatric Genomics Consortium.

We thank the customers of 23andMe who answered surveys, as well as the employees of 23andMe, who together made this research possible.

See publication for full list of disclosures.

Subjects:

Research Funding:

See publication for full funding statement.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Genetics & Heredity
  • DEFICIT HYPERACTIVITY DISORDER
  • LD SCORE REGRESSION
  • ASSOCIATION METAANALYSIS
  • GENETIC ARCHITECTURE
  • PROVIDES INSIGHTS
  • MAJOR DEPRESSION
  • SEXUAL-BEHAVIOR
  • POLYGENIC RISK
  • IDENTIFIES 11
  • US CHILDREN

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

Show all authors Show less authors

Journal Title:

Nature Genetics

Volume:

Volume 51, Number 1

Publisher:

, Pages 63-+

Type of Work:

Article | Post-print: After Peer Review

Abstract:

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 ADHD sample and a meta-analysis of quantitative measures of ADHD symptoms in the population, support these findings while highlighting study-specific differences on genetic overlap with educational attainment. Strong concordance with GWAS of quantitative population measures of ADHD symptoms supports that clinical diagnosis of ADHD is an extreme expression of continuous heritable traits.

Copyright information:

© 2018, The Author(s), under exclusive licence to Springer Nature America, Inc.

Export to EndNote