J Korean Neuropsychiatr Assoc.
2008 Jan;47(1):73-80.
Association between Alpha-1C-Adrenergic Receptor Gene and Attention Deficit Hyperactivity Disorder
- Affiliations
-
- 1Department of Psychiatry, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea. adore412@paran.com
- 2Department of Preventive Medicine, School of Medicine, Eulji University, Daejeon, Korea.
- 3Department of Pharmacology, School of Medicine, Eulji University, Daejeon, Korea.
- 4LabGenomics Clinical Research Institute, LabGenomics, Seoul, Korea.
- 5Department of Psychiatry, Seoul National University Bundang Hospital, Seongnam, Korea.
- 6Department of Psychiatry, Kyungpook National University Hospital, Daegu, Korea.
- 7Department of Psychiatry, Chungbuk National University Hospital, Cheongju, Korea.
- 8Department of Psychiatry, Chonbuk National University Hospital, Jeonju, Korea.
Abstract
OBJECTIVES
Neurobiological and pharmacological research has suggested that the dysregulation of the central noradrenergic systems might be involved in the pathophysiology of ADHD. The aim of this study was to examine the association of the alpha- 1C-adrenergic receptor gene (ADRA1C) with ADHD in Korean subjects.
METHODS
In a case-control study, we assessed 186 DSM-IV ADHD probands and 150 normal controls. One hundred and eight trios were studied in a family-based association analysis. Psychiatric diagnoses were derived through structured diagnostic interviews. For the clinical evaluation of the ADHD subjects, the Child Behavior Checklist (CBCL), the ADHD Rating Scale-IV (ARS) and the Junior Temperament and Character Inventory (JTCI) were administered. A computerized continuous performance test (CPT) was used to measure the inattention and impulsivity of the ADHD children.
RESULTS
There were no significant differences in the genotype or allele frequencies of the ADRA1C PstI polymorphism between the ADHD and control group (p<0.05). The transmission disequilibrium test (TDT) analysis observed no evidence for biased transmission of any of the alleles of the PstI polymorphism. There were no significant differences in the CPT or JTCI profiles between those ADHD subjects with the CC genotype and those with the other (CT+TT) genotypes at the PstI polymorphism.
CONCLUSION
The results of this study do not support the ADRA1C as a major genetic susceptibility factor in ADHD.
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