Association studies of −3081(A/T) polymorphism of norepinephrine transporter gene with attention deficit/hyperactivity disorder in Korean population

Recent studies showing the improvement of ADHD symptoms obtained with the highly selective noradrenergic reuptake inhibitor, atomoxetine, demonstrate that the noradrenergic system plays the role of pathophysiology in this disorder. It is revealed that the norepinephrine transporter gene (SLC6A2) is...

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Veröffentlicht in:American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2010-03, Vol.153B (2), p.691-694
Hauptverfasser: Joung, Yoosook, Kim, Chun-Hyung, Moon, Jisook, Jang, Won-Seok, Yang, Jaewon, Shin, Dongwon, Lee, Soonyoung, Kim, Kwang-Soo
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Sprache:eng
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Zusammenfassung:Recent studies showing the improvement of ADHD symptoms obtained with the highly selective noradrenergic reuptake inhibitor, atomoxetine, demonstrate that the noradrenergic system plays the role of pathophysiology in this disorder. It is revealed that the norepinephrine transporter gene (SLC6A2) is a possible candidate gene directly related to ADHD. To determine possible roles of the SLC6A2 as a susceptibility gene for ADHD, we performed the genetic association study for a functional −3081(A/T) polymorphism, located in the promoter region of SLC6A2. For the present study of association between ADHD and the SLC6A2, 103 male patients with ADHD and 103 normal male controls were randomly gathered. Significant differences were found in the allele frequencies (χ2 = 5.60, P = 0.02) and the odds ratio for the allele T between the ADHD and normal subjects was 1.59 (95% CI: 1.08–2.34) suggesting that T allele is critical to make the group difference. Significant group difference was also found in AA, AT, TT genotypes (χ2 = 7.1, P = 0.02). The odds ratio for TT and AT genotypes was 4.57 (95% CI: 2.56–8.15) and 1.96 (95% CI: 0.96–3.78), respectively. Findings in the present study provided further evidence of association between ADHD and −3081(A/T) polymorphism of SLC6A2. © 2009 Wiley‐Liss, Inc.
ISSN:1552-4841
1552-485X
DOI:10.1002/ajmg.b.31012