A family based study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD)

Turic, D., Williams, H., Langley, K., Owen, M., Thapar, A. and O'Donovan, M.C. (2005) A family based study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD). American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 133B, (1), 64-67. (doi:10.1002/ajmg.b.30123).


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Neurobiological studies have suggested that altered dopaminergic function may contribute to the etiology of attention deficit hyperactivity disorder (ADHD). The gene encoding catechol-O-methyltransferase (COMT) is an attractive candidate for ADHD susceptibility as it plays a major role in the degradation of dopamine. Moreover, a functional Val158Met polymorphism in COMT that alters the activity of the encoded protein has been strongly implicated in frontal lobe function, with the high activity Valine allele being associated with poorer performance, and ADHD is thought to involve fronto-striatal pathways. We have examined this functional variant for association with ADHD in a family based association sample comprising 279 probands and their parents. We have also examined two other markers in the COMT gene (rs737865, rs165599) which, together with the Val/Met variant, have recently been shown to be associated with altered COMT expression rather than enzyme activity. No evidence for association was observed with any single marker or haplotype in a sample of 279 affected children and their parents

Item Type: Article
Digital Object Identifier (DOI): doi:10.1002/ajmg.b.30123
ISSNs: 1552-4841 (print)
1552-485X (electronic)
Related URLs:
Keywords: catechol-O-methyltransferase (COMT), attention deficit hyperactivity disorder (ADHD, association, polymorphisms
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
B Philosophy. Psychology. Religion > BF Psychology
Divisions : University Structure - Pre August 2011 > School of Psychology > Division of Clinical Neuroscience
ePrint ID: 148369
Accepted Date and Publication Date:
February 2005Published
Date Deposited: 29 Jun 2010 13:34
Last Modified: 31 Mar 2016 13:22
URI: http://eprints.soton.ac.uk/id/eprint/148369

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