Molecular genetic contribution to the developmental course of attention-deficit hyperactivity disorder
Open accessAbstract
Objective The developmental trajectory of attention-deficit hyperactivity disorder (ADHD) is variable. Utilizing a longitudinally assessed sample, we investigated the contribution of susceptibility gene variants, previously implicated through pooled or meta-analyses, to the developmental course of Attention-Deficit Hyperactivity Disorder over time.Methods 151 children (aged 6-12) who met diagnostic criteria for ADHD were assessed using research diagnostic interviews during childhood and 5 years later in adolescence. Severity was defined as total number of ADHD symptoms at baseline and reassessment. Association with variants at DRD4, DRD5, and the dopamine transporter gene, DAT was analyzed using linear regression.Results As expected, affected individuals showed a decline in ADHD severity over time. The DRD4 48 bp VNTR 7-repeat and DRD5 CA(n) microsatellite marker 148 bp risk alleles were associated with persistent ADHD. Those possessing the DRD4 7 repeat risk allele showed less of a decline in severity at reassessment than those without the risk allele.Conclusions Those carrying the DRD4 7 risk allele showed greater symptom severity at follow-up and less ADHD reduction over time. These findings support the hypothesis that some susceptibility genes for ADHD also influence its developmental course.
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Evidence on the association of the DRD4 7-repeat allele with persistent ADHD is inconsistent, with some studies finding an association and others finding that patients with persistent ADHD symptoms were less likely to have the allele.
“Some studies have found that the DRD4 7-repeat (7R) allele was associated with persistent ADHD (Biederman et al., 2009; Langley et al., 2009), while other studies found that the patients with persistent ADHD symptoms were less likely have DRD4 7R allele (Shaw et al., 2007).”
From A Review of Heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD) (2019) · cites this paper as Langley et al., 2009
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- Authors
- Langley, K., Fowler, T. A., Grady, D. L., Moyzis, R. K., Holmans, P. A., van den Bree, M. B. M., Owen, M. J., O’Donovan, M. C., & Thapar, A.
- Affiliations
- Cardiff University (GB)
- University of California, Irvine (US)
- Corresponding author
- Langley, Kate
- Venue
- European Child & Adolescent Psychiatry
- Published
- 2008-06-18
- Volume
- 18
- Issue
- 1
- Pages
- 26-32
- ISSN
- 1018-8827 (ISSN-L)
- 1435-165X
- OpenAlex
- W2049631179
- Cited by
- 47
- References
- 38
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 2 · 2019: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 6 · 2012: 4
- FWCI
- 4.67
- Type
- journal article
- Language
- en
- Open access
- green
- hal.science
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- European Child & Adolescent Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Social Science Open Access Repository (GESIS – Leibniz Institute for the Social Sciences) (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- attention deficit hyperactivity disorder, developmental course, symptom severity, DRD5, dopamine transporter gene, DAT, genetic susceptibility, persistent ADHD, children and adolescents, longitudinal follow-up
- MeSH terms
- Adolescent, Age Factors, Alleles, Attention Deficit Disorder with Hyperactivity, Child, Diagnosis, Differential, Humans, Molecular Biology, Genetic Variation, Disease Progression, Dopamine Plasma Membrane Transport Proteins, Receptors, Dopamine D4, Receptors, Dopamine D5
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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