Association between prenatal stress and infant DNA methylation

CAMILA ZELGERT; BIBIANA FABRE; FRASCH, MARTIN G.; MARTA C. ANTONELLI; PETER ZIMMERMANN; RORY WILSON; MELANIE WALDENBERGER; RITIKA SHARMA; BERG, G.; JENNIFER KRIEBEL; LOBMAIER, SILVIA M.

Congreso; European Human Genetics Conference; 2020

Introduction: Maternal stress before and during pregnancy can profoundly affect the in-utero and postnatal child development. We hypothesize that children affected by prenatal stress and thus epigenetic reprogramming might show alterations of the fetal autonomic nervous system and Hypothalamic- Pituitary axis. Methods: We evaluated epigenome-wide methylation sites in the saliva of infants born to stressed and non-stressed mothers. In a prospective study of expecting mothers, we screened women for chronic stress exposure at the 28thweek using the Cohen Perceived Stress Scale (PSS) and Prenatal Distress questionnaires (PDQ). Expectant mothers were classified into the stressed group (SG, PSS-10 ≥ 19, N= 55); the control group (CG, PSS-10 < 19, N=55) matched 1:1 for parity, maternal age and gestational age. On the day of delivery, maternal blood and maternal head hair were collected for cortisol measurements. DNAmethylation was measured in saliva samples of the newborn using the EPIC Bead Chip array (758132 CpG). In order to identify associations between cortisol and methylation, linear regression models adjusting for confounders (sex, age and smoking) were run. Results: Cortisol measurements were 63% higher in SG versus CG. The top hit of the regression analysis is cg15652683 (p = 2.16e-06), a CpG annotated to VIPR2 gene (Chr 7q36.3) that function as neurotransmitters and neuroendocrine hormones. Conclusion: Our work is ongoing and aims tosee if the prenatal stress can be employed as a predictive biomarker of child neurodevelopmental outcome.