1. Association study of GIT1 gene with attention-deficit hyperactivity disorder in Brazilian children and adolescents.
- Author
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Salatino-Oliveira, A., Genro, J. P., Chazan, R., Zeni, C., Schmitz, M., Polanczyk, G., Roman, T., Rohde, L. A., and Hutz, M. H.
- Subjects
ADOLESCENT psychopathology ,ATTENTION-deficit hyperactivity disorder ,CHILDREN with attention-deficit hyperactivity disorder ,DISEASE prevalence ,G protein coupled receptors ,SINGLE nucleotide polymorphisms ,GENE expression ,MEDICAL statistics - Abstract
Attention-deficit hyperactivity disorder ( ADHD) is one of the most common psychiatric disorders in children with a worldwide prevalence of 5.3%. Recently, a Korean group assessed the G-protein-coupled receptor kinase-interacting protein 1 ( GIT1) gene that had previously been associated with ADHD. In their work, 27 single nucleotide polymorphisms SNPs in the GIT1 gene were tested; however, only the rs550818 SNP was associated with ADHD susceptibility. Moreover, the presence of the risk-associated allele determined reduced GIT1 expression, and Git1-deficient mice exhibit ADHD-like phenotypes. The aim of this study was to determine if this association also occurs in a sample of Brazilian children with ADHD. No effect of GIT1 genotypes on ADHD susceptibility was observed in the case-control analysis. The odds ratios ( ORs) were 0.75 ( P = 0.184) for the CT genotype and 1.09 ( P = 0.862) for the TT genotype. In addition, the adjusted OR of the CT+ TT genotypes vs. the CC genotype was also estimated ( P = 0.245). There were no dimensional associations between the GIT1 genotypes and both hyperactivity and /impulsivity, and only hyperactivity Swanson, Nolan and Pelham Scale-Version IV ( SNAP-IV) scores ( P = 0.609 and P = 0.247, respectively). The transmission/disequilibrium test indicated that there was no over-transmission of rs550818 alleles from parents to ADHD children ( z = 0.305; P = 0.761). We conclude that rs550818 is not associated with ADHD in this Brazilian sample. More studies are required before concluding that this polymorphism plays a role in ADHD susceptibility. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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