Molecular Psychiatry
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January 1998, Volume 3, Number 1, Pages 38-41
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Immediate communication
Association of the dopamine receptor D4 (DRD4) gene with a refined phenotype of attention deficit hyperactivity disorder (ADHD): a family-based approach
J M Swanson1, G A Sunohara2, J L Kennedy2, R Regino1, E Fineberg1, T Wigal1, M Lerner1, L Williams1, G J LaHoste1 and S Wigal1

1The Child Development Center, Department of Pediatrics, University of California, Irvine, 19722 MacArthur Boulevard, Irvine, CA 92612, USA

2Neurogenetics Section, The Clarke Institute of Psychiatry, University of Toronto, R-30, 250 College Street, Ontario, Canada M5T 1R8

Abstract

Previously in this journal, we reported an association of the dopamine D4 receptor gene (DRD4) and attention deficit hyperactivity disorder (ADHD). In a population-association (case-control) study of 39 children with a refined phenotype of ADHD and 39 ethnically matched controls, we observed an increased percentage of the 7 repeat allele (29% vs 12%) and the 7+ genotype (49% vs 21%) in the ADHD group compared to the control group. In a replication and an extension of our initial study, we recruited another sample of ADHD subjects and found percentages of the 7 repeat allele (28%) and the 7+ genotype (48%) consistent with our previous findings. We used a family-based approach to evaluate a predicted association of DRD4 and ADHD based on a test of allele transmission focused on the 7 repeat allele. We identified 52 families based on the diagnosis of the refined phenotype of ADHD in the proband and the availability of DNA from both biological parents as well as the proband. Haplotype relative risk (HRR) analysis was performed to test our a priori hypothesis and produced significant results (chi-square = 4.65, P < 0.035). this provides additional evidence that the drd4 gene is associated with a refined phenotype of adhd.

Keywords

attention deficit hyperactivity disorder; dopamine; DRD4; genetics

Received 15 October 1997; revised 30 October 1997; accepted 31 October 1997
January 1998, Volume 3, Number 1, Pages 38-41
Table of contents    Previous  Abstract  Next   Article  PDF