Fetal growth compromise moderates associations between SNPs within angiogenic and neurotrophic genes and AD/HD symptom severity

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Taylor F. Smith (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Arthur Anastopoulos

Abstract: Low birth weight, a form of fetal growth compromise, is a well-established risk factor for Attention-Deficit/Hyperactivity Disorder (AD/HD; Nigg, Nikolas, & Burt, 2010); however, it is unclear how birth weight moderates genetic risk for AD/HD. From a Developmental Origins of Health and Disease (Gluckman & Hanson, 2004) framework, this study investigated if fetal growth compromise moderated relationships between SNPs within angiogenic, dopaminergic and neurotrophic genes and AD/HD symptom severity. A total of 398 youth from two multi-site, family-based studies of AD/HD were included in the current analysis. Results demonstrated that fetal growth compromise moderated associations between SNPs within angiogenic (HIF1A and NRP1) and a neurotrophic gene (NTRK3), but not dopamine genes, and AD/HD symptom severity. The gene x environment interactions remained significant after controlling for SNPs associated with birth weight and adjusting for multiple testing. Taken together, findings may suggest that prenatal ischemia/hypoxia is an environmental pathogen for AD/HD which confers vulnerability for the disorder through regulating the expression of angiogenic and neurotrophic genes.

Additional Information

Language: English
Date: 2012
ADHD, Angiogenic, Birth weight, Developmental origins, Gene-environment interaction, Neurotrophic
Attention-deficit hyperactivity disorder $x Genetic aspects
Birth weight, Low $x Health aspects
Genotype-environment interaction

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