Journal
MOLECULAR PSYCHIATRY
Volume 15, Issue 9, Pages 928-937Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2009.22
Keywords
prenatal smoking; MAOA; gene x environment interaction; developmental psychopathology
Funding
- NIDA [DA15223]
- National Institute for Health Research [CSA/03/07/014] Funding Source: researchfish
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Genetic susceptibility to antisocial behavior may increase fetal sensitivity to prenatal exposure to cigarette smoke. Testing putative gene x exposure mechanisms requires precise measurement of exposure and outcomes. We tested whether a functional polymorphism in the gene encoding the enzyme monoamine oxidase A (MAOA) interacts with exposure to predict pathways to adolescent antisocial behavior. We assessed both clinical and information-processing outcomes. One hundred seventy-six adolescents and their mothers participated in a follow-up of a pregnancy cohort with well-characterized exposure. A sex-specific pattern of gene x exposure interaction was detected. Exposed boys with the low-activity MAOA 5' uVNTR (untranslated region variable number of tandem repeats) genotype were at increased risk for conduct disorder (CD) symptoms. In contrast, exposed girls with the high-activity MAOA uVNTR genotype were at increased risk for both CD symptoms and hostile attribution bias on a face-processing task. There was no evidence of a gene-environment correlation (rGE). Findings suggest that the MAOA uVNTR genotype, prenatal exposure to cigarettes and sex interact to predict antisocial behavior and related information-processing patterns. Future research to replicate and extend these findings should focus on elucidating how gene x exposure interactions may shape behavior through associated changes in brain function. Molecular Psychiatry (2010) 15, 928-937; doi:10.1038/mp.2009.22; published online 3 March 2009
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