Linked Life Data

11864723

Source:http://linkedlifedata.com/resource/pubmed/id/11864723

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2002-2-26
pubmed:abstractText
Convincing data support the hypothesis that genetic factors are involved in the etiology of attention-deficit hyperactivity disorder (ADHD). Various lines of evidence have shown that the dopamine system plays a crucial role in the pathophysiology of ADHD. The dopamine D3 receptor gene (DRD3) represents a promising candidate to examine in ADHD. Animal studies have shown that DRD3 mRNA is highly expressed in the ventral striatum suggesting an involvement of this receptor in the control of motor behaviour. Manipulation of DRD3 in rodents has led to a mouse model with nonfunctional D3 receptors that displays hyperactive behaviour in various environmental conditions. Furthermore, administration of 7-OH-DPAT, a dopaminergic agonist that binds preferentially to D3 receptors exerts an inhibitory effect on locomotor activity while D3 antagonists induce hyperactivity. Among various polymorphisms described for DRD3, the BalI polymorphism is most interesting because it codes for an aminoacid substitution in the N-terminus of the receptor. The receptor products of the two alleles (Ser/Gly) exhibit differential affinity for dopamine. To determine if DRD3 Ser9/Gly is involved in the susceptibility to ADHD we genotyped 39 adults with ADHD and their respective parents (trios). Adult ADHD represents a promising phenotype for studying the genetic component of the disorder. In fact, a recent family study has shown that relatives of adult ADHD patients have a higher rate of ADHD compared to relatives of children with ADHD suggesting a stronger genetic component for the adult version. The results of genotyping in the 39 trios analyzed with the transmission disequilibrium test showed no excess of transmission for DRD3 MscI/BalI alleles (chi(2) = 0.360; df = 1; P = 0.54). This result, although from a relatively small sample, indicates that it is unlikely that DRD3 is playing a major role in the etiology of ADHD in our sample.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0166-4328
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
A transmission disequilibrium test of the Ser9/Gly dopamine D3 receptor gene polymorphism in adult attention-deficit hyperactivity disorder.
pubmed:affiliation
Department of Psychiatry, Neurogenetics Section, Centre for Addiction and Mental Health, Clarke Site, University of Toronto, 250 College Street R-30, Ont, Canada M5T 1R8.
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, Non-U.S. Gov't