ADHDgene Database

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Large-scale studies

Data Summary

Published Variant
- SNP: 1391
- CNV: 398
- Others: 173
Published Gene: 359
Published Region: 128
Pathway by PBA: 8
Study: 361

Study Report

Basic Info

Reference	Muglia P, 200211864723
Citation	Muglia P., Jain U. and Kennedy J. L. (2002) "A transmission disequilibrium test of the Ser9/Gly dopamine D3 receptor gene polymorphism in adult attention-deficit hyperactivity disorder." Behav Brain Res, 130(1-2): 91-5.
Study Design	family-based
Study Type	Candidate-gene association study
Sample Size	39 nuclear families
Predominant Ethnicity	Canadian
Population	Canada
Age Group	Adults

Detail Info

Summary	To determine if DRD3 Ser9/Gly is involved in the susceptibility to ADHD they 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 (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.
Total Sample	39 nuclear families of adult ADHD probands were analyzed for this study consisting of 25 families with both parental DNAs genotyped, and 14 families with DNA available for a single parent. In six families one of the parents was also affected by ADHD and in one family both parents were affected.
Sample Collection	Patients were referred from primary care practitioners in the Toronto area to the Adult and Adolescent ADHD Research Program of the Centre for Addiction and Mental Health (CAMH), Clarke Site, at the University of Toronto in Toronto, Ontario. The patient was then asked to come to the Clinic where informed consent was obtained and a self-report questionnaire was completed. The study was approved by the University and CAMH human subjects ethics committee. Once the questionnaire was completed, the subjects were entered into a weekly psychoeducational program that included a simulated classroom.
Diagnosis Description	The patient was required to meet the Diagnostic and Statistical Manual, 4th ed. childhood ADHD criteria thresholds for ADHD on all the following questionnaires: (a) >46 on the Wender Utah Rating Scale; (b) >55 on the Brown Attention Deficit Disorder Scale; (c) >60 on the Conner's Adult ADHD Rating Scale. Further details on the clinical assessment were published previously.
Technique	Blood samples were drawn from patients and relatives and the DNA was extracted from whole blood following a nonenzymatic, high salt method. A 462 bp segment of the first exon of DRD3 that contain the BalI/MscI polymorphism was amplified by polymerase chain reaction (PCR). PCR products were digested overnight with 1 U of MscI endonuclease (isoschizomer of BalI). Digested products were separated and visualised in a 3.0% agarose gel prepared with ethidium bromide. Depending on the absence or presence of the MscI restriction sites different fragment sizes were present. Genotyping was performed according to the original description of the BalI/MscI polymorphism by Lannfelt et al..
Analysis Method	The genotypes in the nuclear families were analysed using the transmission disequilibrium test.
Result Description	Results from TDT analysis did not show significant biased transmission for the BalI/MscI DRD3 polymorphism alleles (X²=0.360; df=1; P=0.54).

Other variant reported by this study (count: 1)

Genes reported by this study (count: 1)