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Author Notes:

Correspondence to: Michelle M. Martel, mmartel@uno.edu.

We are indebted to the families and staff who made this study possible.

Subjects:

Research Funding:

This research was supported by NIH National Institute of Mental Health Grants R01-MH63146, MH59105, and MH70542.

Keywords:

  • Adolescent
  • Attention Deficit Disorder with Hyperactivity
  • Attention Deficit and Disruptive Behavior Disorders
  • Case-Control Studies
  • Child
  • Family Conflict
  • Female
  • Genotype
  • Homozygote
  • Humans
  • Male
  • Parenting
  • Polymorphism, Genetic
  • Promoter Regions, Genetic
  • Receptors, Dopamine D4
  • Surveys and Questionnaires
  • Tandem Repeat Sequences

The dopamine receptor D4 gene (DRD4) moderates family environmental effects on ADHD

Tools:

Journal Title:

Journal of Abnormal Child Psychology

Volume:

Volume 39, Number 1

Publisher:

, Pages 1-10

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Attention-Deficit/Hyperactivity Disorder (ADHD) is a prime candidate for exploration of gene-by-environment interaction (i.e., G x E), particularly in relation to dopamine system genes, due to strong evidence that dopamine systems are dysregulated in the disorder. Using a G x E design, we examined whether the DRD4 promoter 120-bp tandem repeat polymorphism, previously associated with ADHD, moderated the effects of inconsistent parenting and marital conflict on ADHD or Oppositional-Defiant Disorder (ODD). Participants were 548 children with ADHD and non-ADHD comparison children and their parents. Homozygosity for the DRD4 promoter 120-bp tandem repeat insertion allele increased vulnerability for ADHD and ODD only in the presence of inconsistent parenting and appeared to increase susceptibility to the influence of increased child self-blame for marital conflict on ADHD inattention. DRD4 genotypes may interact with these proximal family environmental risk factors by increasing the individual's responsivity to environmental contingencies. © 2010 Springer Science+Business Media, LLC.

Copyright information:

© 2010 Springer Science+Business Media, LLC.

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