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.
Original language | English (US) |
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Pages (from-to) | 83-90 |
Number of pages | 8 |
Journal | Cognitive, Affective and Behavioral Neuroscience |
Volume | 9 |
Issue number | 1 |
DOIs | |
State | Published - Mar 2009 |
ASJC Scopus subject areas
- Cognitive Neuroscience
- Behavioral Neuroscience