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A drosophila model for attention deficit hyperactivity disorder (ADHD): No evidence of association with PRKG1 gene
Authors:De Luca Vincenzo  Muglia Pierandrea  Jain Umesh  Basile Vincenzo S  Sokolowski Marla B  Kennedy James L
Affiliation:(1) Neurogenetics Section, University of Toronto, Toronto, Ontario, Canada;(2) Adult ADHD Clinic, Clarke Site, Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada;(3) Department of Psychiatry, Second University of Naples, Naples, Italy;(4) Department of Zoology, University of Toronto at Mississauga, Mississauga, Ontario
Abstract:
Attention deficit hyperactivity disorder (ADHD) is a prevalent psychiatric condition in children and follow up studies have indicated that 22–33% of patients continue to suffer from ADHD during late adolescence and adulthood. The action of psychostimulant drugs may be determined by additional mechanisms beyond the dopamine transporter and receptors. We are exploring new methodology for discovering these mechanisms. For example, in Drosophila, such an additional determinant of psychostimulant action could be protein kinase G (PKG) that affects food-search behavior. Here we initiated studies with the human homologue of PKG, the PRKG1 gene. The aim of this study was to investigate for the presence of linkage disequilibrium between the protein kinase G gene (PRKG1) and adult ADHD in a sample of nuclear families. Genotyping data for the C2276T polymorphism were analyzed using the Transmission Disequilibrium Test (TDT). Sixty three nuclear families were informative for the TDT on C2276T polymorphism, which showed no preferential transmission of either allele (chi-square=0.778, df=1, p=0.316). These findings exclude a direct involvement of this genetic marker of the Protein kinase G gene in the pathogenesis of ADHD.
Keywords:Adult ADHD  PRKG1 (protein kinase G gene)  PKG (CGMP-dependent protein kinase)  polymorphism  linkage disequilibrium  TDT (transmission/disequilibrium test)  genetics
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