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

A family based study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD)
A family based study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD)
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
catechol-O-methyltransferase (COMT), attention deficit hyperactivity disorder (ADHD, association, polymorphisms
1552-4841
64-67
Turic, D.
492e37c3-c13b-4c7e-a73f-076525e9e3f1
Williams, H.
39faaeb7-9127-4890-bbf0-3c3785a4ed57
Langley, K.
ce8d5c40-3372-4746-a091-55f787db296f
Owen, M.
df950252-ab3c-4cfb-a73c-c31adafe8983
Thapar, A.
792558b3-01ec-4ccf-83c6-9f408aa3b601
O'Donovan, M.C.
07541263-71ea-4d7e-ba4e-2ced1268be5a
Turic, D.
492e37c3-c13b-4c7e-a73f-076525e9e3f1
Williams, H.
39faaeb7-9127-4890-bbf0-3c3785a4ed57
Langley, K.
ce8d5c40-3372-4746-a091-55f787db296f
Owen, M.
df950252-ab3c-4cfb-a73c-c31adafe8983
Thapar, A.
792558b3-01ec-4ccf-83c6-9f408aa3b601
O'Donovan, M.C.
07541263-71ea-4d7e-ba4e-2ced1268be5a

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).

Record type: Article

Abstract

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

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More information

Published date: February 2005
Keywords: catechol-O-methyltransferase (COMT), attention deficit hyperactivity disorder (ADHD, association, polymorphisms

Identifiers

Local EPrints ID: 148369
URI: http://eprints.soton.ac.uk/id/eprint/148369
ISSN: 1552-4841
PURE UUID: 3710d4ba-0038-4e3b-9071-c589de911158

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Date deposited: 29 Jun 2010 13:34
Last modified: 14 Mar 2024 01:02

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Contributors

Author: D. Turic
Author: H. Williams
Author: K. Langley
Author: M. Owen
Author: A. Thapar
Author: M.C. O'Donovan

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