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Attention-deficit/hyperactivity disorder phenotype is influenced by a functional catechol-O-methyltransferase variant

  • Biological Child and Adolescent Psychiatry - Original Article
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Abstract

The catechol-O-methyltransferase gene (COMT) plays a crucial role in the metabolism of catecholamines in the frontal cortex. A single nucleotide polymorphism (Val158Met 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 Val158Met 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 Val158Met 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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Acknowledgments

We thank the children and their families for their participation in the study and Ulrike Schülter for expert technical assistance. Bernd Janthur, MD, Child Psychiatrist, Dillingen, Germany closely cooperated with this project. This research was supported by the German Research Organisation (Deutsche Forschungsgemeinschaft, DFG) by grants ME 1923/5-1, ME 1923/5-3, and GRK 1389/1.

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Correspondence to Christine M. Freitag.

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Pálmason, H., Moser, D., Sigmund, J. et al. Attention-deficit/hyperactivity disorder phenotype is influenced by a functional catechol-O-methyltransferase variant. J Neural Transm 117, 259–267 (2010). https://doi.org/10.1007/s00702-009-0338-2

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  • DOI: https://doi.org/10.1007/s00702-009-0338-2

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