Molecular genetics of adult ADHD: converging evidence from genome-wide association and extended pedigree linkage studies
Open accessAbstract
A genome-wide association (GWA) study with pooled DNA in adult attention-deficit/hyperactivity disorder (ADHD) employing approximately 500K SNP markers identifies novel risk genes and reveals remarkable overlap with findings from recent GWA scans in substance use disorders. Comparison with results from our previously reported high-resolution linkage scan in extended pedigrees confirms several chromosomal loci, including 16q23.1-24.3 which also reached genome-wide significance in a recent meta-analysis of seven linkage studies (Zhou et al. in Am J Med Genet Part B, 2008). The findings provide additional support for a common effect of genes coding for cell adhesion molecules (e.g., CDH13, ASTN2) and regulators of synaptic plasticity (e.g., CTNNA2, KALRN) despite the complex multifactorial etiologies of adult ADHD and addiction vulnerability.
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CDH13 was putatively associated with depression and has been implicated in ADHD.
“The cadherin 13 (CDH13) gene, which codes for cell adhesion molecules, was found to be putatively associated with depression and has also been implicated in ADHD 32.”
From Genome-wide meta-analysis of depression identifies 102 independent variants and highlights the importance of the prefrontal brain regions (2019) · cites this paper as [32]
ASTN2 was putatively associated with depression and is involved in ADHD aetiology and neuronal development.
“A further gene involved in cell adhesion, astrotactin 2 (ASTN2), which we found to be putatively associated with depression is also involved in ADHD aetiology 32 and plays a role in neuronal development in the brain 33.”
From Genome-wide meta-analysis of depression identifies 102 independent variants and highlights the importance of the prefrontal brain regions (2019) · cites this paper as [32]
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- Authors
- Lesch, K.-P., Timmesfeld, N., Renner, T. J., Halperin, R., Röser, C., Nguyen, T. T., Craig, D. W., Romanos, J., Heine, M., Meyer, J., Freitag, C., Warnke, A., Romanos, M., Schäfer, H., Walitza, S., Reif, A., Stephan, D. A., & Jacob, C.
- Affiliations
- University of Würzburg (DE)
- Philipps University of Marburg (DE)
- Translational Genomics Research Institute (US)
- Universität Trier (DE)
- Universitätsklinikum des Saarlandes (DE)
- Corresponding author
- Lesch, Klaus-Peter
- ORCID
- Venue
- Journal of Neural Transmission
- Published
- 2008-10-07
- Volume
- 115
- Issue
- 11
- Pages
- 1573-1585
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- OpenAlex
- W2066179547
- Cited by
- 374
- References
- 59
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 7 · 2023: 8 · 2022: 14 · 2021: 15 · 2020: 22 · 2019: 18 · 2018: 23 · 2017: 28 · 2016: 27 · 2015: 33 · 2014: 26 · 2013: 26 · 2012: 31
- FWCI
- 18.92
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neural Transmission (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- 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 › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- adult ADHD, attention deficit hyperactivity disorder, genome-wide association study, linkage analysis, extended pedigrees, substance use disorders, risk genes, adhesion molecules, CDH13, ASTN2, synaptic plasticity, CTNNA2, KALRN, addiction vulnerability, multifactorial etiology
- MeSH terms
- Adult, Attention Deficit Disorder with Hyperactivity, Chromosomes, DNA, Female, Genotype, Humans, Genetic Linkage, Male, Molecular Biology, Neuronal Plasticity, Cell Adhesion Molecules, Genome, Human, Polymorphism, Single Nucleotide, Genome-Wide Association Study
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