Linked Life Data

15635644

Source:http://linkedlifedata.com/resource/pubmed/id/15635644

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-1-26
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1552-4841
pubmed:author
pubmed:copyrightInfo
(c) 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
133B
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
64-7
pubmed:dateRevised
2008-5-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
A family based study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD).
pubmed:affiliation
Department of Psychological Medicine, University of Wales College of Medicine, Cardiff, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't