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Brain Network Connectivity and Association with Catechol-O-Methyltransferase Gene Polymorphism in Korean
Jeong Ha Park1, Young Don Son2, Yeni Kim3
1Department of Psychiatry, Woorisoa Children's Hospital, Seoul, Republic of Korea.
Children with attention-deficit hyperactivity disorder (ADHD) show altered brain connectivity in the default mode network (DMN) and dorsal attention network (DAT). This connectivity is further influenced by catechol-O-methyltransferase (COMT) gene variations.
Area of Science:
- Neuroscience
- Genetics
- Child Psychology
Background:
- Attention-deficit hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder.
- The default mode network (DMN) and dorsal attention network (DAT) are crucial for cognitive functions.
- Catechol-O-methyltransferase (COMT) gene polymorphism is implicated in various neurological conditions.
Purpose of the Study:
- To investigate the relationship between COMT gene polymorphism and brain connectivity within and between the DMN and DAT in children with ADHD.
- To compare brain connectivity patterns in children with ADHD and healthy controls (HCs).
Main Methods:
- Functional magnetic resonance imaging (fMRI) was used to assess resting-state brain connectivity.
- COMT genotyping was performed to identify valine carriers and methionine homozygotes.
- Standardized cognitive and psychological assessments were administered to all participants.
Main Results:
- Children with ADHD exhibited increased functional connectivity (FC) within the DMN and DAT compared to HCs.
- COMT gene variations were associated with altered FC within and between the DMN and DAT in children with ADHD.
- Specific patterns of FC were observed in valine carriers versus methionine homozygotes, both in ADHD and HC groups.
Conclusions:
- Brain connectivity within the DMN and DAT is increased in children with ADHD.
- COMT gene polymorphism significantly influences DMN and DAT connectivity in children with ADHD.
- These findings highlight the interplay between genetic factors and neural network alterations in ADHD pathogenesis.
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