PubMed · 16919150
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A C Baverstock, F Finlay. 2006. ADHD abroad.. https://doi.org/10.1111/j.1365-2214.2006.00649.x
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The dopamine transporter (DAT) plays a key role in the regulation of dopaminergic neurotransmission and is also the major site of action for methylphenidate which is one of the main drugs used to treat attention deficit hyperactivity disorder (ADHD). Most association studies with ADHD have concentrated on the 3'-untranslated region of the gene (3'-UTR) mainly in a variable number of tandem repeat (VNTR) polymorphism, but these investigations have reported discordant results. In this study, we tested this VNTR polymorphism and an additional promoter polymorphism -839 C>T (Rs: 2652511) using family-based association analyses in a sample of 243 Brazilian ADHD children and adolescents and their parents. No significant linkage disequilibrium between the two polymorphisms was detected in this sample (D' = 0.56; P = 0.22). No evidence of association with the VNTR polymorphism was found. A significant association (P = 0.03) for biased transmission of the C allele at the -839 C>T polymorphism to ADHD children in the total sample was observed, which was strengthened when the analyses were restricted to the ADHD combined type (P = 0.004). Our results suggest a role for the promoter region of DAT1 gene in ADHD susceptibility in this Brazilian sample.
Solute carrier 6 (SLC6) is a gene family of ion-coupled plasma membrane cotransporters, including transporters of neurotransmitters, amino acids, and osmolytes that mediate the movement of their substrates into cells to facilitate or regulate synaptic transmission, neurotransmitter recycling, metabolic function, and fluid homeostasis. Polymorphisms in transporter genes may influence expression and activity of transporters and contribute to behavior, traits, and disease. Determining the relationship between the monoamine transporters and complex psychiatric disorders has been a particular challenge that is being met by evolving approaches. Elucidating the functional consequences of and interactions among polymorphic sites is advancing our understanding of this relationship. Examining the influence of environmental influences, especially early-life events, has helped bridge the gap between genotype and phenotype. Refining phenotypes, through assessment of endophenotypes, specific behavioral tasks, medication response, and brain network properties has also improved detection of the impact of genetic variation on complex behavior and disease.
OBJECTIVES: This study is the first to investigate EEG coherence differences between two groups of children with attention-deficit/hyperactivity disorder combined type (AD/HD), with or without comorbid oppositional defiant disorder (ODD), and normal control subjects. METHODS: Each group consisted of 20 males. All subjects were between the ages of 8 and 12 years, and groups were matched on age. EEG was recorded during an eyes-closed resting condition from 21 monopolar derivations. Wave-shape coherence was calculated for 8 intrahemispheric electrode pairs (4 in each hemisphere), and 8 interhemispheric electrode pairs, within each of the delta, theta, alpha, and beta bands. RESULTS: Children with comorbid AD/HD and ODD had intrahemispheric coherences at shorter inter-electrode distances significantly reduced from those apparent in children with AD/HD without comorbid ODD. Such reduced coherences in the comorbid group appeared to wash out coherence elevations previously noted in AD/HD studies. CONCLUSIONS: The present results suggest that, rather than suffering an additional deficit, children with AD/HD and comorbid ODD show significantly less CNS impairment than AD/HD patients without comorbid ODD. SIGNIFICANCE: These results have treatment implications, suggesting that behavioural training, perhaps using family-based cognitive behavioural therapy, could be useful for those children with AD/HD and comorbid ODD. This should focus on the ODD symptoms, in association with a medication regime focussed on the AD/HD symptoms.