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No evidence of an association between norepinephrine transporter gene polymorphisms and attention deficit hyperactivity disorder: a family-based and case-control association study in a Korean sample

Cited 25 time in Web of Science Cited 26 time in Scopus
Authors
Cho, Soo-Churl; Kim, Jae-Won; Kim, Boong-Nyun; Hwang, Jun-Won; Park, Mira; Kim, Soon Ae; Cho, Dae-Yeon; Yoo, Hee-Jeong; Chung, Un-Sun; Son, Jung-Woo; Park, Tae-Won
Issue Date
2008-06-17
Publisher
Karger
Citation
Neuropsychobiology 2008;57(3):131-138
Keywords
AdolescentAsian Continental Ancestry Group/geneticsAttention/*physiologyAttention Deficit and Disruptive BehaviorDisorders/classification/*geneticsCase-Control StudiesChi-Square DistributionChildChild, PreschoolFemale*Genetic Predisposition to DiseaseHumansKoreaLinkage DisequilibriumMaleNorepinephrine Plasma Membrane Transport Proteins/*geneticsPedigreePolymorphism, Single NucleotideReference ValuesTemperament/*physiology
Abstract
Neurobiological and pharmacological research has suggested that dysregulation of the central noradrenergic systems might be involved in the pathophysiology of attention deficit hyperactivity disorder (ADHD). Previous studies have demonstrated that the norepinephrine transporter gene (SLC6A2) is associated with ADHD. The aims of this study were to examine the association of the SLC6A2 G1287A and -3081(A/T) polymorphisms with ADHD in Korean children and adolescents, and to determine the relationships of the genotypes of these two polymorphisms with continuous performance test results and the Junior Temperament and Character Inventory profiles of ADHD. In a case-control study, we assessed 186 ADHD probands and 150 normal controls; 109 trios were studied in a family-based association analysis. There were no significant differences in the genotype or allele frequencies of the SLC6A2 G1287A and -3081(A/T) polymorphisms between the ADHD and control groups (p > 0.05). In the transmission disequilibrium test analyses, there was no evidence for biased transmission of any of the alleles of the SLC6A2 G1287A and -3081(A/T) polymorphisms. In the haplotype analyses of these two polymorphisms, the global and individual chi(2) tests showed no significant associations between any of the haplotypes and ADHD. There were no significant differences with respect to the continuous performance test results and the Junior Temperament and Character Inventory profiles in the ADHD probands according to the genotypes of the SLC6A2 G1287A and -3081(A/T) polymorphisms. Our findings do not support SLC6A2 as a major genetic susceptibility factor in ADHD.
ISSN
1423-0224 (Electronic)
Language
English
URI
https://hdl.handle.net/10371/67515
DOI
https://doi.org/10.1159/000138916
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College of Medicine/School of Medicine (의과대학/대학원)Psychiatry (정신과학전공)Journal Papers (저널논문_정신과학전공)
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