Journal of Clinical Epigenetics Open Access

  • ISSN: 2472-1158
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Epigenetic marks of prenatal maternal stress

2nd International Congress on Epigenetics & Chromatin
November 06-08, 2017 | Frankfurt, Germany

Stephan Claes

University of Leuven, Belgium

Scientific Tracks Abstracts: J Clin Epigenet

Abstract:

According to the Dohad (developmental origins of health and disease) hypothesis, the prenatal environment has a major influence on the liability of the individual to develop somatic or psychiatric disorders later in life. In a prospective study, we examined levels of anxiety and depression, as well as cortisol secretion, in pregnant women at three different time points during gestation. Subsequently, we analyzed the methylation status of the DNA of the newborn. We further examined stress sensitivity in the babies until the age of 1 year. We first examined methylation patterns of the promoter region of two candidate genes, NR3C1 and IGF2. For these genes, methylation differences in the newborn have been described in relation to prenatal stress and to prenatal famine respectively. We found that prenatal stress, more specifically prenatal anxiety, was associated with changes in DNA methylation at birth. Subsequently, we examined epigenome-wide methylation in the DNA of the newborn applying the Illumina 450K chip. Using two independent analysis methods, we found the GABA receptor 1B (GABBR1) gene to be differentially methylated because of prenatal maternal anxiety. Further, we established a link between GABBR1 methylation at birth and stress system activity (cortisol secretion both basally and in response to stress) of the babies at 2, 4 and 12 months of age. In conclusion, we confirm the role of prenatal maternal anxiety in determining methylation patterns in the newborn and establish the GABBR1 gene as a potential candidate gene regulating stress reactivity in the young child. Recent Publications 1. Van Assche E, Claes S. (2016). Depressive symptoms in adolescence: The role of perceived parental support, psychological control, and proactive control in interaction with 5-HTTLPR. Euro Psychiatry. 35: 55-63. 2. Moons T, Claes S. (2016). Genetic Evaluation of Schizophrenia Using the Illumina Human Exome Chip. PLoS One. 30; 11: e0150464. 3. Vangeel EB, Claes S. (2015). DNA methylation in imprinted genes IGF2 and GNASXL is associated with prenatal maternal stress. Genes Brain Behav. 14: 573-82. 4. Humps T, Claes S. (2013). Investigating the influence of maternal cortisol and emotional state during pregnancy on the DNA methylation status of the glucocorticoid receptor gene (NR3C1) promoter region in cord blood. J Psychiatr Res. 47: 880-91. 5. Vrieze E, Claes S. (2013). Reduced reward learning predicts outcome in major depressive disorder. Biol Psychiatry. 73: 639-45.

Biography :

Stephan Claes is Professor of Psychiatry and Head of the Adult Psychiatry service at the University Psychiatric Hospital KU Leuven, Belgium. He heads a research group called GRASP (Genetic Research about Stress and Psychiatry), which focuses on genetic and epigenetic determinants of stress sensitivity, and on the link between stress sensitivity and mood disorders. He is a Senior Clinical Investigator of the Fund for Scientific Research Flanders, and has co-authored over 100 publications.