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	Renner, T. J., 201121739117
Citation	Renner T. J., Nguyen T. T., Romanos M., Walitza S., Roser C., Reif A., Schafer H., Warnke A., Gerlach M. and Lesch K. P. (2011) "No evidence for association between a functional promoter variant of the Norepinephrine Transporter gene SLC6A2 and ADHD in a family-based sample." Atten Defic Hyperact Disord, 3(3): 285-9.
Study Design	family-based
Study Type	Candidate-gene association study
Sample Size	235 children from 162 families
Predominant Ethnicity	Caucasian
Population	German
Gender	178 boys
Age Group	Children/Adolescents : The mean age of the affected children was 11.03 years (SD: 3.12 years).

Detail Info

Summary	Due to its influence on catecholaminergic signaling, variants of the coding gene (SLC6A2) have been widely investigated in ADHD. Several previous studies report an association between single nucleotide polymorphisms located in SLC6A2 and ADHD; however, the findings are inconsistent. The variant A-3081T (rs28386840) has been shown to have major influence on the expression levels of SLC6A2 due to sequence alteration at a repressor binding site, with the T-allele being associated with ADHD. We tested this potential association of A-3081T in a German family-based ADHD sample of 235 children from 162 families, which has a power >99% based on the previously reported odds ratios. There was no evidence for an overtransmission of the risk allele T (transmission rate: 48.5%, P = 0.55).
Total Sample	Two hundred and thirty-five children (178 boys) with ADHD from 162 families were recruited and phenotypically characterized by a team of experienced child and adolescent psychiatrists in the outpatient unit of the Department of Child and Adolescent Psychiatry and Psychotherapy, University of Wurzburg, according to DSM-IV criteria American Psychiatric Association. Families were included if they had one or more children affected with ADHD to perform family-based association and genome-wide linkage studies. The index patient was required to be older than 8 years and to fulfill DSM-IV criteria for the combined subtype, and further affected siblings had to be at least 6 years of age. In 107 families one child, in 40 families two, in 12 families three and in 3 families four affected children were recruited.
Sample Collection	Two hundred and thirty-five children (178 boys) with ADHD from 162 families were recruited and phenotypically characterized by a team of experienced child and adolescent psychiatrists in the outpatient unit of the Department of Child and Adolescent Psychiatry and Psychotherapy, University of Wurzburg.
Diagnosis Description	Two hundred and thirty-five children with ADHD from 162 families were recruited according to DSM-IV criteria American Psychiatric Association.
Technique	To genotype the variant A-3081T (rs28386840), polymerase chain reaction was performed as described by Kim et al.
Analysis Method	The two-sided pedigree disequilibrium test weighting on family size (PDT-sum) was performed to assess the transmission rates and to test for association. A nominal p-value lower than 0.05 was considered statistically significant.
Result Description	We tested this potential association of A-3081T in a German family-based ADHD sample of 235 children from 162 families, which has a power>99% based on the previously reported odds ratios. There was no evidence for an overtransmission of the risk allele T (transmission rate: 48.5%, P = 0.55). We conclude that A-3081T is not a major risk variant in our ADHD sample, though SLC6A2 remains an interesting candidate gene in ADHD, especially for the inattentive subtype.

SNPs reported by this study (count: 1)

Genes reported by this study (count: 1)