Attention-deficit/hyperactivity disorder phenotype is influenced by a functional catechol-O-methyltransferase variant
Abstract
The catechol-O-methyltransferase gene (COMT) plays a crucial role in the metabolism of catecholamines in the frontal cortex. A single nucleotide polymorphism (Val(158)Met SNP, rs4680) leads to either methionine (Met) or valine (Val) at codon 158, resulting in a three- to fourfold reduction in COMT activity. The aim of the present study was to assess the COMT Val(158)Met SNP as a risk factor for attention-deficit/hyperactivity disorder (ADHD), ADHD symptom severity and co-morbid conduct disorder (CD) in 166 children with ADHD. The main finding of the present study is that the Met allele of the COMT Val(158)Met SNP was associated with ADHD and increased ADHD symptom severity. No association with co-morbid CD was observed. In addition, ADHD symptom severity and early adverse familial environment were positive predictors of lifetime CD. These findings support previous results implicating COMT in ADHD symptom severity and early adverse familial environment as risk factors for co-morbid CD, emphasizing the need for early intervention to prevent aggressive and maladaptive behavior progressing into CD, reducing the overall severity of the disease burden in children with ADHD.
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The Met-allele is associated with increased risk for ADHD in children in a predominantly male (84%) sample.
“A recent study confirmed the association of the Met-allele with increased risk for ADHD in children in a predominantly male (84%) sample, and also reported that Met was associated with increased symptom severity (Pálmason et al, 2010).”
From DAT1 and COMT effects on delay discounting and trait impulsivity in male adolescents with attention deficit/hyperactivity disorder and healthy controls (2010) · cites this paper as Pálmason et al, 2010
Met is associated with increased symptom severity.
“A recent study confirmed the association of the Met-allele with increased risk for ADHD in children in a predominantly male (84%) sample, and also reported that Met was associated with increased symptom severity (Pálmason et al, 2010).”
From DAT1 and COMT effects on delay discounting and trait impulsivity in male adolescents with attention deficit/hyperactivity disorder and healthy controls (2010) · cites this paper as Pálmason et al, 2010
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References 67 · Cited by 44
- Authors
- Pálmason, H., Moser, D., Sigmund, J., Vogler, C., Hänig, S., Schneider, A., Seitz, C., Marcus, A., Meyer, J., & Freitag, C. M.
- Affiliations
- Universität Trier (DE)
- University of Basel (CH)
- Universitätsklinikum des Saarlandes (DE)
- Klinikum Mutterhaus der Borromäerinnen (DE)
- Goethe University Frankfurt (DE)
- Corresponding author
- Freitag, Christine M.
- Venue
- Journal of Neural Transmission
- Published
- 2009-11-28
- Volume
- 117
- Issue
- 2
- Pages
- 259-267
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- OpenAlex
- W2050364492
- Cited by
- 44
- References
- 67
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 1 · 2021: 2 · 2020: 2 · 2016: 1 · 2015: 5 · 2014: 3 · 2013: 5 · 2012: 6
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neural Transmission (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- attention deficit hyperactivity disorder, catechol-O-methyltransferase, COMT Val158Met polymorphism, ADHD symptom severity, conduct disorder, comorbidities, catecholamine metabolism, family environment, children, genetic risk factors
- MeSH terms
- Adolescent, Alleles, Attention Deficit Disorder with Hyperactivity, Catechol O-Methyltransferase, Child, Environment, Family, Female, Humans, Male, Phenotype, Psychiatric Status Rating Scales, Risk Factors, Comorbidity, Sequence Analysis, DNA, Conduct Disorder, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide
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