Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder

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Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder. / Rajagopal, Veera M.; Duan, Jinjie; Vilar-Ribó, Laura; Grove, Jakob; Zayats, Tetyana; Ramos-Quiroga, J. Antoni; Satterstrom, F. Kyle; Artigas, María Soler; Bybjerg-Grauholm, Jonas; Bækvad-Hansen, Marie; Als, Thomas D.; Rosengren, Anders; Daly, Mark J; Neale, Benjamin M; Nordentoft, Merete; Werge, Thomas; Mors, Ole; Hougaard, David M.; Mortensen, Preben B.; Ribasés, Marta; Børglum, Anders D.; Demontis, Ditte.

I: Nature Genetics, Bind 54, Nr. 8, 2022, s. 1117-1124.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Rajagopal, VM, Duan, J, Vilar-Ribó, L, Grove, J, Zayats, T, Ramos-Quiroga, JA, Satterstrom, FK, Artigas, MS, Bybjerg-Grauholm, J, Bækvad-Hansen, M, Als, TD, Rosengren, A, Daly, MJ, Neale, BM, Nordentoft, M, Werge, T, Mors, O, Hougaard, DM, Mortensen, PB, Ribasés, M, Børglum, AD & Demontis, D 2022, 'Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder', Nature Genetics, bind 54, nr. 8, s. 1117-1124. https://doi.org/10.1038/s41588-022-01143-7

APA

Rajagopal, V. M., Duan, J., Vilar-Ribó, L., Grove, J., Zayats, T., Ramos-Quiroga, J. A., Satterstrom, F. K., Artigas, M. S., Bybjerg-Grauholm, J., Bækvad-Hansen, M., Als, T. D., Rosengren, A., Daly, M. J., Neale, B. M., Nordentoft, M., Werge, T., Mors, O., Hougaard, D. M., Mortensen, P. B., ... Demontis, D. (2022). Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder. Nature Genetics, 54(8), 1117-1124. https://doi.org/10.1038/s41588-022-01143-7

Vancouver

Rajagopal VM, Duan J, Vilar-Ribó L, Grove J, Zayats T, Ramos-Quiroga JA o.a. Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder. Nature Genetics. 2022;54(8):1117-1124. https://doi.org/10.1038/s41588-022-01143-7

Author

Rajagopal, Veera M. ; Duan, Jinjie ; Vilar-Ribó, Laura ; Grove, Jakob ; Zayats, Tetyana ; Ramos-Quiroga, J. Antoni ; Satterstrom, F. Kyle ; Artigas, María Soler ; Bybjerg-Grauholm, Jonas ; Bækvad-Hansen, Marie ; Als, Thomas D. ; Rosengren, Anders ; Daly, Mark J ; Neale, Benjamin M ; Nordentoft, Merete ; Werge, Thomas ; Mors, Ole ; Hougaard, David M. ; Mortensen, Preben B. ; Ribasés, Marta ; Børglum, Anders D. ; Demontis, Ditte. / Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder. I: Nature Genetics. 2022 ; Bind 54, Nr. 8. s. 1117-1124.

Bibtex

@article{d945c8e632ea472fbc573d9921eda093,

title = "Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder",

abstract = "Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with onset in childhood (childhood ADHD); two-thirds of affected individuals continue to have ADHD in adulthood (persistent ADHD), and sometimes ADHD is diagnosed in adulthood (late-diagnosed ADHD). We evaluated genetic differences among childhood (n = 14,878), persistent (n = 1,473) and late-diagnosed (n = 6,961) ADHD cases alongside 38,303 controls, and rare variant differences in 7,650 ADHD cases and 8,649 controls. We identified four genome-wide significant loci for childhood ADHD and one for late-diagnosed ADHD. We found increased polygenic scores for ADHD in persistent ADHD compared with the other two groups. Childhood ADHD had higher genetic overlap with hyperactivity and autism compared with late-diagnosed ADHD and the highest burden of rare protein-truncating variants in evolutionarily constrained genes. Late-diagnosed ADHD had a larger genetic overlap with depression than childhood ADHD and no increased burden in rare protein-truncating variants. Overall, these results suggest a genetic influence on age at first ADHD diagnosis, persistence of ADHD and the different comorbidity patterns among the groups.",

author = "Rajagopal, {Veera M.} and Jinjie Duan and Laura Vilar-Rib{\'o} and Jakob Grove and Tetyana Zayats and Ramos-Quiroga, {J. Antoni} and Satterstrom, {F. Kyle} and Artigas, {Mar{\'i}a Soler} and Jonas Bybjerg-Grauholm and Marie B{\ae}kvad-Hansen and Als, {Thomas D.} and Anders Rosengren and Daly, {Mark J} and Neale, {Benjamin M} and Merete Nordentoft and Thomas Werge and Ole Mors and Hougaard, {David M.} and Mortensen, {Preben B.} and Marta Ribas{\'e}s and B{\o}rglum, {Anders D.} and Ditte Demontis",

note = "Publisher Copyright: {\textcopyright} 2022, The Author(s), under exclusive licence to Springer Nature America, Inc.",

year = "2022",

doi = "10.1038/s41588-022-01143-7",

language = "English",

volume = "54",

pages = "1117--1124",

journal = "Nature Genetics",

issn = "1061-4036",

publisher = "nature publishing group",

number = "8",

}

RIS

TY - JOUR

T1 - Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder

AU - Rajagopal, Veera M.

AU - Duan, Jinjie

AU - Vilar-Ribó, Laura

AU - Grove, Jakob

AU - Zayats, Tetyana

AU - Ramos-Quiroga, J. Antoni

AU - Satterstrom, F. Kyle

AU - Artigas, María Soler

AU - Bybjerg-Grauholm, Jonas

AU - Bækvad-Hansen, Marie

AU - Als, Thomas D.

AU - Rosengren, Anders

AU - Daly, Mark J

AU - Neale, Benjamin M

AU - Nordentoft, Merete

AU - Werge, Thomas

AU - Mors, Ole

AU - Hougaard, David M.

AU - Mortensen, Preben B.

AU - Ribasés, Marta

AU - Børglum, Anders D.

AU - Demontis, Ditte

PY - 2022

Y1 - 2022

N2 - Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with onset in childhood (childhood ADHD); two-thirds of affected individuals continue to have ADHD in adulthood (persistent ADHD), and sometimes ADHD is diagnosed in adulthood (late-diagnosed ADHD). We evaluated genetic differences among childhood (n = 14,878), persistent (n = 1,473) and late-diagnosed (n = 6,961) ADHD cases alongside 38,303 controls, and rare variant differences in 7,650 ADHD cases and 8,649 controls. We identified four genome-wide significant loci for childhood ADHD and one for late-diagnosed ADHD. We found increased polygenic scores for ADHD in persistent ADHD compared with the other two groups. Childhood ADHD had higher genetic overlap with hyperactivity and autism compared with late-diagnosed ADHD and the highest burden of rare protein-truncating variants in evolutionarily constrained genes. Late-diagnosed ADHD had a larger genetic overlap with depression than childhood ADHD and no increased burden in rare protein-truncating variants. Overall, these results suggest a genetic influence on age at first ADHD diagnosis, persistence of ADHD and the different comorbidity patterns among the groups.

AB - Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with onset in childhood (childhood ADHD); two-thirds of affected individuals continue to have ADHD in adulthood (persistent ADHD), and sometimes ADHD is diagnosed in adulthood (late-diagnosed ADHD). We evaluated genetic differences among childhood (n = 14,878), persistent (n = 1,473) and late-diagnosed (n = 6,961) ADHD cases alongside 38,303 controls, and rare variant differences in 7,650 ADHD cases and 8,649 controls. We identified four genome-wide significant loci for childhood ADHD and one for late-diagnosed ADHD. We found increased polygenic scores for ADHD in persistent ADHD compared with the other two groups. Childhood ADHD had higher genetic overlap with hyperactivity and autism compared with late-diagnosed ADHD and the highest burden of rare protein-truncating variants in evolutionarily constrained genes. Late-diagnosed ADHD had a larger genetic overlap with depression than childhood ADHD and no increased burden in rare protein-truncating variants. Overall, these results suggest a genetic influence on age at first ADHD diagnosis, persistence of ADHD and the different comorbidity patterns among the groups.

U2 - 10.1038/s41588-022-01143-7

DO - 10.1038/s41588-022-01143-7

M3 - Journal article

C2 - 35927488

AN - SCOPUS:85135556379

VL - 54

SP - 1117

EP - 1124

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

IS - 8

ER -

ID: 321821432