Genome-wide analysis of attention deficit hyperactivity disorder in Norway
Open accessAbstract
BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is a highly heritable neuropsychiatric condition, but it has been difficult to identify genes underlying this disorder. This study aimed to explore genetics of ADHD in an ethnically homogeneous Norwegian population by means of a genome-wide association (GWA) analysis followed by examination of candidate loci. MATERIALS AND METHODS: Participants were recruited through Norwegian medical and birth registries as well as the general population. Presence of ADHD was defined according to DSM-IV criteria. Genotyping was performed using Illumina Human OmniExpress-12v1 microarrays. Statistical analyses were divided into several steps: (1) genome-wide association in the form of logistic regression in PLINK and follow-up pathway analyses performed in DAPPLE and INRICH softwares, (2) SNP-heritability calculated using genome-wide complex trait analysis (GCTA) tool, (3) gene-based association tests carried out in JAG software, and (4) evaluation of previously reported genome-wide signals and candidate genes of ADHD. RESULTS: In total, 1.358 individuals (478 cases and 880 controls) and 598.384 autosomal SNPs were subjected to GWA analysis. No single polymorphism reached genome-wide significance. The strongest signal was observed at rs9949006 in the ENSG00000263745 gene (OR=1.51, 95% CI 1.28-1.79, p=1.38E-06). Pathway analyses of the top SNPs implicated genes involved in the regulation of gene expression, cell adhesion and inflammation. Among previously identified ADHD candidate genes, prominent association signals were observed for SLC9A9 (rs1393072, OR=1.46, 95% CI = 1.21-1.77, p=9.95E-05) and TPH2 (rs17110690, OR = 1.38, 95% CI = 1.14-1.66, p=8.31E-04). CONCLUSION: This study confirms the complexity and heterogeneity of ADHD etiology. Taken together with previous findings, our results point to a spectrum of biological mechanisms underlying the symptoms of ADHD, providing targets for further genetic exploration of this complex disorder.
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Genetic studies have found associations between polymorphisms in inflammatory pathway genes and ADHD.
“GWAS studies have identified associations between ADHD and the gene for IL-1RA (Segman et al., 2002) as well as genes involved in regulation of gene expression, cell adhesion, and inflammation (Zayats et al., 2015).”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Zayats et al., 2015
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- Authors
- Zayats, T., Athanasiu, L., Sonderby, I., Djurovic, S., Westlye, L. T., Tamnes, C. K., Fladby, T., Aase, H., Zeiner, P., Reichborn-Kjennerud, T., Knappskog, P. M., Knudsen, G. P., Andreassen, O. A., Johansson, S., & Haavik, J.
- Affiliations
- University of Bergen (NO)
- Oslo University Hospital (NO)
- University of Oslo (NO)
- Norwegian Institute of Public Health (NO)
- Haukeland University Hospital (NO)
- Corresponding author
- Zayats, Tetyana
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-04-13
- Volume
- 10
- Issue
- 4
- Pages
- e0122501
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4395400
- OpenAlex
- W2095280681
- Cited by
- 83
- References
- 86
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 6 · 2022: 5 · 2021: 5 · 2020: 8 · 2019: 11 · 2018: 15 · 2017: 11 · 2016: 9 · 2015: 5
- FWCI
- 10.83
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by)
- BIBSYS Brage (BIBSYS (Norway)) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- NORA - Norwegian Open Research Archives (submittedVersion, other-oa)
- Figshare (submittedVersion, cc-by)
- Funders
- European Commission (602805)
- Norges Forskningsråd (223273, 213837, 151918/S10, 2013-123)
- National Institutes of Health (FP7/2007-2013, 223273, 2013-123, NO-ES-75558, n01es75558-11-0-1, 213837)
- National Institute of Neurological Disorders and Stroke (1-UO1-NS-047537, UO1-NS-047537, 047537-01, UO1 NS 047537–01, NS 047537, U01NS047537, 1 UO1 NS 047537‐01, FP7/2007-2013)
- National Institute of Environmental Health Sciences (ES-75558, UO1 NS 047537-01, NO-ES-75558, N01 ES075558, 1 UO1 NS 047537-01, N0-ES-75 558)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- attention deficit hyperactivity disorder, ADHD genetics, genome-wide association study, candidate genes, SLC9A9, tryptophan hydroxylase 2, gene expression regulation, cell adhesion, inflammation, heritability, pathway analysis, Norwegian population
- MeSH terms
- Attention Deficit Disorder with Hyperactivity, Genotype, Humans, Phenotype, Tryptophan Hydroxylase, Sodium-Hydrogen Exchangers, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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