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	Laurin N, 2008(c)17948899
Citation	Laurin N., Ickowicz A., Pathare T., Malone M., Tannock R., Schachar R., Kennedy J. L. and Barr C. L. (2008) "No evidence for genetic association between DARPP-32 (PP1R1B) polymorphisms and attention deficit hyperactivity disorder." Am J Med Genet B Neuropsychiatr Genet, 147(3): 339-42.
Study Design	family-based
Study Type	Candidate-gene association study
Sample Size	255 probands and 53 affected siblings
Predominant Ethnicity	Caucasian
Population	Canada
Age Group	Children/Adolescents : 7-16 years

Detail Info

Summary	Here, they tested the DARPP-32 gene, PPP1R1B, for association with ADHD using four polymorphic markers selected across the gene in a sample of 255 ADHD families. They did not detect evidence of association of individual marker alleles and haplotype analysis did not reveal significant association in this sample of families. Moreover, they found no relationship between the same alleles or haplotypes and symptom scores of inattention or hyperactivity/ impulsivity in these families using a quantitative approach. In conclusion, albeit a key regulatory role in dopamine signaling, their data do not support a major contribution of the DARPP-32 gene in ADHD.
Total Sample	255 probands and 53 affected siblings between 7 and 16 years old were included
Diagnosis Description	255 probands and 53 affected siblings between 7 and 16 years old were included if they met DSM-IV criteria for one of the three ADHD subtypes (predominantly inattentive, predominantly hyperactive/impulsive or combined). The methods of assessment, characteristics of the subjects, and inclusion/ exclusion criteria have been described previously, including the instruments used to collect information for the diagnosis of ADHD and co-morbid conditions [Quist et al., 2000; Laurin et al., 2005].
Technique	DNA was extracted from blood lymphocytes using a high salt extraction method [Miller et al. 1988]. The markers were genotyped using Assay-on-demand SNP genotyping and the ABI 7900-HT Sequence Detection System.
Analysis Method	The TDTphase program from the UNPHASED package and the TRANSMIT program were used to test for biased transmission of alleles or haplotypes, respectively. Quantitative trait TDT analyses were carried out using the FBAT program v1.5.5, with the additive model of inheritance.
Result Description	They did not detect evidence of association of individual marker alleles and haplotype analysis did not reveal significant association in this sample of families. Moreover, they found no relationship between the same alleles or haplotypes and symptom scores of inattention or hyperactivity/ impulsivity in these families using a quantitative approach.

SNPs reported by this study (count: 4)

SNP	Allele Change	Risk Allele	Statistical Values	Author Comments	Result of Statistical Analysis
rs1495099	G/C		P-value=0.586, X² (1 df)=0.297 in the categorical analysis; P-value>0.05 in the quantitative analysis	no significant evidence of association no significant evidence of association	Non-significant
rs879606	G/A		P-value=0.442, X² (1 df)=0.593 in the categorical analysis; P-value>0.05 in the quantitative analysis	no significant evidence of association no significant evidence of association	Non-significant
rs3764352	T/C		P-value=0.865, X² (1 df)=0.029 in the categorical analysis; P-value>0.05 in the quantitative analysis	no significant evidence of association no significant evidence of association	Non-significant
rs907094	A/G		P-value=0.933, X² (1 df)=0.007 in the categorical analysis; P-value>0.05 in the quantitative analysis	no significant evidence of association no significant evidence of association	Non-significant

Genes reported by this study (count: 1)