Epigenome-wide association study of attention-deficit/hyperactivity disorder in adults
Rovira, Paula (Hospital Universitari Vall d'Hebron)
Sánchez-Mora, Cristina (Universitat de Barcelona. Departament de Genètica, Microbiologia i Estadística)
Pagerols, Mireia (Hospital Universitari Vall d'Hebron)
Richarte, Vanesa (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Corrales, Montserrat (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Fadeuilhe, Christian (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Vilar-Ribó, L (Hospital Universitari Vall d'Hebron)
Arribas, Lorena (Hospital Universitari Vall d'Hebron)
Shireby, Gemma (University of Exeter. University of Exeter Medical School)
Hannon, Eilis (University of Exeter)
Mill, Jonathan (University of Exeter)
Casas Brugué, Miquel (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Ramos-Quiroga, Josep Antoni (Universitat Autònoma de Barcelona. Departament de Psiquiatria i de Medicina Legal)
Soler Artigas, María (Universitat de Barcelona. Departament de Genètica, Microbiologia i Estadística)
Ribasés Haro, Marta (Universitat de Barcelona. Departament de Genètica, Microbiologia i Estadística)

Date:	2020
Abstract:	Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder that often persists into adulthood. There is growing evidence that epigenetic dysregulation participates in ADHD. Given that only a limited number of epigenome-wide association studies (EWASs) of ADHD have been conducted so far and they have mainly focused on pediatric and population-based samples, we performed an EWAS in a clinical sample of adults with ADHD. We report one CpG site and four regions differentially methylated between patients and controls, which are located in or near genes previously involved in autoimmune diseases, cancer or neuroticism. Our sensitivity analyses indicate that smoking status is not responsible for these results and that polygenic risk burden for ADHD does not greatly impact the signatures identified. Additionally, we show an overlap of our EWAS findings with genetic signatures previously described for ADHD and with epigenetic signatures for smoking behavior and maternal smoking. These findings support a role of DNA methylation in ADHD and emphasize the need for additional efforts in larger samples to clarify the role of epigenetic mechanisms on ADHD across the lifespan.
Grants:	Ministerio de Economía, Industria y Competitividad CP09/00119 Ministerio de Economía, Industria y Competitividad CPII15/00023 Agència de Gestió d'Ajuts Universitaris i de Recerca 2016FI_B 00899 Ministerio de Economía, Industria y Competitividad CD15/00199 Instituto de Salud Carlos III FI18/0028 European Commission. Horizon 2020 667302 European Commission. Horizon 2020 728018 Ministerio de Economía, Industria y Competitividad PI15/01789 Ministerio de Economía, Industria y Competitividad PI16/01505 Instituto de Salud Carlos III PI17/00289 Instituto de Salud Carlos III PI18/01788 Instituto de Salud Carlos III PI19/00721 Instituto de Salud Carlos III PI19/01224 Agència de Gestió d'Ajuts Universitaris i de Recerca 2017SGR146
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	ADHD ; Genetics
Published in:	Translational psychiatry, Vol. 10 (june 2020) , ISSN 2158-3188

DOI: 10.1038/s41398-020-0860-4
PMID: 32561708

12 p, 784.2 KB

The record appears in these collections:
Articles > Research articles
Articles > Published articles