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

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. / ADHD Working Group of the Psychiatric Genomics Consortium (PGC).

In: Nature Genetics, Vol. 51, No. 1, 01.2019, p. 63-75.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

ADHD Working Group of the Psychiatric Genomics Consortium (PGC) 2019, 'Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder', Nature Genetics, vol. 51, no. 1, pp. 63-75. https://doi.org/10.1038/s41588-018-0269-7

APA

ADHD Working Group of the Psychiatric Genomics Consortium (PGC) (2019). Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics, 51(1), 63-75. https://doi.org/10.1038/s41588-018-0269-7

Vancouver

ADHD Working Group of the Psychiatric Genomics Consortium (PGC). Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics. 2019 Jan;51(1):63-75. https://doi.org/10.1038/s41588-018-0269-7

Author

ADHD Working Group of the Psychiatric Genomics Consortium (PGC). / Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. In: Nature Genetics. 2019 ; Vol. 51, No. 1. pp. 63-75.

Bibtex

@article{3dc9f896bc5a4ebe99833749672fd781,
title = "Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder",
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.",
keywords = "Adolescent, Attention Deficit Disorder with Hyperactivity/genetics, Brain/physiology, Child, Child, Preschool, Cohort Studies, Female, Gene Expression Regulation/genetics, Genetic Loci/genetics, Genetic Predisposition to Disease/genetics, Genome-Wide Association Study/methods, Humans, Male, Polymorphism, Single Nucleotide/genetics, Risk",
author = "Ditte Demontis and Walters, {Raymond K} and Joanna Martin and Manuel Mattheisen and Als, {Thomas D} and Esben Agerbo and G{\'i}sli Baldursson 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 Goldstein, {Jacqueline I} and Grasby, {Katrina L} and Jakob Grove and Gudmundsson, {Olafur O} and Hansen, {Christine S} and Hauberg, {Mads Engel} and Hollegaard, {Mads V} and Howrigan, {Daniel P} and Hailiang Huang and Maller, {Julian B} and Martin, {Alicia R} and Martin, {Nicholas G} and Jennifer Moran and Jonatan Pallesen and Palmer, {Duncan S} and Pedersen, {Carsten B{\o}cker} and Pedersen, {Marianne Gi{\o}rtz} and Timothy Poterba and Poulsen, {Jesper Buchhave} and Stephan Ripke and Robinson, {Elise B} and Satterstrom, {F Kyle} and Hreinn Stefansson and Christine Stevens and Patrick Turley and Walters, {G Bragi} and Hyejung Won and Wright, {Margaret J} and Andreassen, {Ole A} and Philip Asherson and Burton, {Christie L} and Boomsma, {Dorret I} and Merete Nordentoft and Thomas Werge and {ADHD Working Group of the Psychiatric Genomics Consortium (PGC)}",
year = "2019",
month = jan,
doi = "10.1038/s41588-018-0269-7",
language = "English",
volume = "51",
pages = "63--75",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder

AU - Demontis, Ditte

AU - Walters, Raymond K

AU - Martin, Joanna

AU - Mattheisen, Manuel

AU - Als, Thomas D

AU - Agerbo, Esben

AU - Baldursson, Gísli

AU - Belliveau, Rich

AU - Bybjerg-Grauholm, Jonas

AU - Bækvad-Hansen, Marie

AU - Cerrato, Felecia

AU - Chambert, Kimberly

AU - Churchhouse, Claire

AU - Dumont, Ashley

AU - Eriksson, Nicholas

AU - Gandal, Michael

AU - Goldstein, Jacqueline I

AU - Grasby, Katrina L

AU - Grove, Jakob

AU - Gudmundsson, Olafur O

AU - Hansen, Christine S

AU - Hauberg, Mads Engel

AU - Hollegaard, Mads V

AU - Howrigan, Daniel P

AU - Huang, Hailiang

AU - Maller, Julian B

AU - Martin, Alicia R

AU - Martin, Nicholas G

AU - Moran, Jennifer

AU - Pallesen, Jonatan

AU - Palmer, Duncan S

AU - Pedersen, Carsten Bøcker

AU - Pedersen, Marianne Giørtz

AU - Poterba, Timothy

AU - Poulsen, Jesper Buchhave

AU - Ripke, Stephan

AU - Robinson, Elise B

AU - Satterstrom, F Kyle

AU - Stefansson, Hreinn

AU - Stevens, Christine

AU - Turley, Patrick

AU - Walters, G Bragi

AU - Won, Hyejung

AU - Wright, Margaret J

AU - Andreassen, Ole A

AU - Asherson, Philip

AU - Burton, Christie L

AU - Boomsma, Dorret I

AU - Nordentoft, Merete

AU - Werge, Thomas

AU - ADHD Working Group of the Psychiatric Genomics Consortium (PGC)

PY - 2019/1

Y1 - 2019/1

N2 - 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.

AB - 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.

KW - Adolescent

KW - Attention Deficit Disorder with Hyperactivity/genetics

KW - Brain/physiology

KW - Child

KW - Child, Preschool

KW - Cohort Studies

KW - Female

KW - Gene Expression Regulation/genetics

KW - Genetic Loci/genetics

KW - Genetic Predisposition to Disease/genetics

KW - Genome-Wide Association Study/methods

KW - Humans

KW - Male

KW - Polymorphism, Single Nucleotide/genetics

KW - Risk

U2 - 10.1038/s41588-018-0269-7

DO - 10.1038/s41588-018-0269-7

M3 - Journal article

C2 - 30478444

VL - 51

SP - 63

EP - 75

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

IS - 1

ER -

ID: 232647457