ArticleNeurotoxicology and teratology2017
Does MAOA increase susceptibility to prenatal stress in young children?
Article in Neurotoxicology and teratology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Effects of a Personalized Stress Management Intervention on Maternal Mental Health: A Randomized Clinical Trial.Archives of women's mental health · 2025Trial
- HealthSense: Unobtrusive Continuous Stress Monitoring Using a Novel Dual ECG-PPG Patch.... International Conference on Wearable and Implantable Body Sensor Networks. International Conference on Wearable and Implantable Body Sensor Networks · 2024Article
- Genome-wide association study identifies a novel maternal gene × stress interaction associated with spontaneous preterm birth.Pediatric research · 2021Article
- Gaining a deeper understanding of social determinants of preterm birth by integrating multi-omics data.Pediatric research · 2021Review
- The role of monoamine oxidase A in the neurobiology of aggressive, antisocial, and violent behavior: A tale of mice and men.Progress in neurobiology · 2020Review
- micro-Stress EMA: A Passive Sensing Framework for Detecting in-the-wild Stress in Pregnant Mothers.Proceedings of the ACM on interactive, mobile, wearable and ubiquitous technologies · 2019Article
- Gene-environment interaction of monoamine oxidase A in relation to antisocial behaviour: current and future directions.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
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Authors and funding
11 authors at 6 institutions in 1 country.
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Abstract
backgroundWe previously demonstrated a gene-by-prenatal-environment interaction whereby the monoamine oxidase A gene (MAOA) modified the impact of prenatal tobacco exposure (PTE) on adolescent disruptive behavior (DB), with the MAOA risk genotype varying by sex. We extend this work by examining whether this mechanism is evident with another common adversity, prenatal stress exposure (PSE), and whether sex differences are present earlier in development in closer proximity to exposure.
methodsParticipants were 281 mothers and their 285 children derived from a prenatal cohort with in-depth prospective measures of PSE and PTE. We assessed DB at age 5 via dimensional developmentally-sensitive measurement. Analyses were stratified by sex based on prior evidence for sex differences.
resultsConcurrent stress exposure predicted DB in children (β=0.310, p=0.001), while main effects of prenatal exposures were seen only in boys. We found a three-way interaction of MAOA×PSE×sex on DB (β=0.813, p=0.022). Boys with MAOA-H had more DB as a function of PSE, controlling for PTE (β=0.774, p=0.015), and as a function of PTE, controlling for PSE (β=0.362, p=0.037). Boys with MAOA-L did not show this susceptibility. MAOA did not interact with PSE (β=-0.133, p=0.561) nor PTE (β=-0.144; p=0.505) in predicting DB in girls. Examination of gene-environment correlation (rGE) showed a correlation between paternal MAOA-L and daughters' concurrent stress exposure (r=-0.240, p=0.013). DISCUSSION: Findings underscore complex mechanisms linking genetic susceptibility and early adverse exposures. Replication in larger cohorts followed from the pregnancy through adolescence is suggested to elucidate mechanisms that appear to have varying developmental expression.
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