Catechol-O-methyltransferase polymorphism modulates cognitive control in children with chromosome 22q11.2 deletion syndrome |
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Authors: | Yukari Takarae Linda Schmidt Flora Tassone Tony J. Simon |
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Affiliation: | (1) Department of Psychiatry and Behavioral Sciences and the Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute, University of California at Davis Health System, 2825 50th Street, Sacramento, CA 95817, USA;(2) Division of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California at Davis, Sacramento, CA 95817, USA |
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Abstract: | Dopamine plays a critical role in regulating neural activity in prefrontal cortex (PFC) and modulates cognition via a hypothesized inverse U function. We investigated PFC function in children with chromosome 22q11.2 deletion syndrome (22q11.2DS) in which one copy of catechol-O-methyltransferase (COMT) is deleted, thereby shifting them toward the lower end of dopamine turnover on the nonlinear function. A common polymorphism with valine to methionine substitution alters COMT activity that results in higher enzyme activity in the valine variant. Twenty-seven children with 22q11.2DS between 7 and 14 years old, and 21 age-matched typically developing children, performed a modified version of the Attention Network Test. Children with a single valine allele showed a reduction in response times when trials with incongruent flankers were repeated, whereas those who were hemizygous for the methionine allele did not show the same context-based response facilitation. Our results support that a single gene, COMT, could modulate PFC-dependent cognition. |
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