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Cereb Cortex. 2017 May 1;27(5):3080-3092. doi: 10.1093/cercor/bhx065.

Effects of Antenatal Maternal Depressive Symptoms and Socio-Economic Status on Neonatal Brain Development are Modulated by Genetic Risk.

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Department of Biomedical Engineering and Clinical Imaging Research Center, National University of Singapore, Singapore 117576, Singapore.
Singapore Institute for Clinical Sciences, Singapore 117609, Singapore.
Departent of Medical Psychology, Charité University Medicine Berlin, Berlin 10117, Germany.
Development, Health and Disease Research Program, Department of Pediatrics, University of California, Irvine, CA 92697, USA.
Department of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University Health System, Singapore 119228, Singapore.
Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA.
Department of Diagnostic and Interventional Imaging, KK Women's and Children's Hospital (KKH), Singapore 229899, Singapore.
Department of Computer Science, University of North Carolina, Chapel Hill, NC 27599, USA.
Department of Psychiatry, University of North Carolina, Chapel Hill, NC 27514, USA.
Ludmer Centre for Neuroinformatics and Mental Health, Douglas Mental Health University Institute, McGill University, Montréal H4H 1R3, Canada.
Sackler Program for Epigenetics & Psychobiology at McGill University, Montréal H4H 1R3, Canada.


This study included 168 and 85 mother-infant dyads from Asian and United States of America cohorts to examine whether a genomic profile risk score for major depressive disorder (GPRSMDD) moderates the association between antenatal maternal depressive symptoms (or socio-economic status, SES) and fetal neurodevelopment, and to identify candidate biological processes underlying such association. Both cohorts showed a significant interaction between antenatal maternal depressive symptoms and infant GPRSMDD on the right amygdala volume. The Asian cohort also showed such interaction on the right hippocampal volume and shape, thickness of the orbitofrontal and ventromedial prefrontal cortex. Likewise, a significant interaction between SES and infant GPRSMDD was on the right amygdala and hippocampal volumes and shapes. After controlling for each other, the interaction effect of antenatal maternal depressive symptoms and GPRSMDD was mainly shown on the right amygdala, while the interaction effect of SES and GPRSMDD was mainly shown on the right hippocampus. Bioinformatic analyses suggested neurotransmitter/neurotrophic signaling, SNAp REceptor complex, and glutamate receptor activity as common biological processes underlying the influence of antenatal maternal depressive symptoms on fetal cortico-limbic development. These findings suggest gene-environment interdependence in the fetal development of brain regions implicated in cognitive-emotional function. Candidate biological mechanisms involve a range of brain region-specific signaling pathways that converge on common processes of synaptic development.


amygdala; cortical thickness; depression; morphological shape; polygenic risk score

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