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	Brown, A. B., 201121596533
Citation	Brown, A. B., J. Biederman, E. Valera, N. Makris, A. Doyle, S. Whitfield-Gabrieli, E. Mick, T. Spencer, S. Faraone and L. Seidman (2011). "Relationship of DAT1 and adult ADHD to task-positive and task-negative working memory networks." Psychiatry Res 193(1): 7-16.
Study Design	case-control
Study Type	Candidate-gene association study
Sample Size	53 cases and 38 controls
Predominant Ethnicity	Caucasian
Gender	26 female cases, 22 female controls
Age Group	Adults : ADHD patients: mean age=33.7, SD=10.5 years of 9R-carriers, mean age=37.6, SD=11.2 years of 10R/10R; Controls: mean age=30.7, SD=9.1 years of 9R-carriers, mean age=31.6, SD=11.2 years of 10R/10R

Detail Info

Summary	In order to understand the potential mediating effects of task-positive and task-negative networks between DAT1 and diagnosis, we tested effects of genotype and diagnosis on regions of positive and negative BOLD signal change (as measured with fMRI) in 53 adults with ADHD and 38 control subjects during a working memory task. We also examined the relationship of these responses to ADHD symptoms. Our results yielded four principal findings: 1) association of the DAT1 9R allele with adult ADHD, 2) marginal DAT1 association with task-related suppression in left medial PFC, 3) marginal genotypexdiagnosis interaction in the dorsal anterior cingulate cortex, and 4) correlation of DMN suppression to ADHD symptoms. These findings replicate the association of the 9R allele with adult ADHD. Further, we show that DMN suppression is likely linked to DAT1 and to severity of inattention in ADHD. DMN may therefore be a target of DAT1 effects, and lie on the path between the gene and inattention in ADHD.
Total Sample	The resulting sample included 91 adult participants: 53 with ADHD, and 38 controls.
Sample Collection	Participants were recruited from Massachusetts General Hospital (MGH) clinics and advertisements posted in the Boston area.
Diagnosis Description	To assess for psychiatric diagnoseswe administered the Structured Clinical Interview for DSM-IV. To assess ADHD, we used a module derived from the Schedule of Affective Disorders and Schizophrenia for School-Age Children-Epidemiologic Version. An ADHD diagnosis was made if the DSM-IV criteria were met in childhood and persisted into adulthood. At the time of the clinical interview, the distribution of ADHD subtypes was: combined, N=17 (32%); inattentive, N=18 (34%); hyperactive/ impulsive, N=1(2%); and remitted, N=17 (32%).
Technique	Genomic DNA (5 ng) was amplified in a 7 ml reaction using HotStarTaq DNA Polymerase (0.2 U), the proprietary HotStarTaq Buffer (1_), dNTPs (200 mM), and the marker specific primers (0.2 mM). Amplified products were pooled and combined with size standard (LIZ-250) before being analyzed on an ABI-3730. GeneMapper v3.5 was used to analyze the raw results from the ABI3730, however, a genotype was not considered final until two technologists had independently checked (and corrected) the GeneMapper results and were in agreement.
Analysis Method	Demographic and behavioral data were analyzed in PASW Statistics 18.0. 2¡Á2 ANOVAs with group (ADHD vs. controls) and genotype (9R-carriers vs. 10R-homozygotes) as fixed factors were run on demographic, clinical, and N-back performance data.
Result Description	Our results yielded four principal findings: 1) association of the DAT1 9R allele with adult ADHD, 2) marginal DAT1 association with task-related suppression in left medial PFC, 3) marginal genotypexdiagnosis interaction in the dorsal anterior cingulate cortex, and 4) correlation of DMN suppression to ADHD symptoms. These findings replicate the association of the 9R allele with adult ADHD. Further, we show that DMN suppression is likely linked to DAT1 and to severity of inattention in ADHD. DMN may therefore be a target of DAT1 effects, and lie on the path between the gene and inattention in ADHD.

Other variant reported by this study (count: 1)

Genes reported by this study (count: 1)