A1 Refereed original research article in a scientific journal
Partial Support for an Interaction Between a Polygenic Risk Score for Major Depressive Disorder and Prenatal Maternal Depressive Symptoms on Infant Right Amygdalar Volumes
Authors: Acosta H, Kantojärvi K, Hashempour N, Pelto J, Scheinin NM, Lehtola SJ, Lewis JD, Fonov VS, Collins DL, Evans A, Parkkola R, Lähdesmäki T, Saunavaara J, Karlsson L, Merisaari H, Karlsson H, Paunio T, Tuulari JJ
Publication year: 2020
Journal: Cerebral Cortex
Journal name in source: Cerebral cortex (New York, N.Y. : 1991)
Journal acronym: Cereb Cortex
Volume: 30
Issue: 12
First page : 6112
Last page: 3134
Number of pages: 14
ISSN: 1047-3211
eISSN: 1460-2199
DOI: https://doi.org/10.1093/cercor/bhaa158(external)
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/49812195(external)
Psychiatric disease susceptibility partly originates prenatally and is shaped by an interplay of genetic and environmental risk factors. A recent study has provided preliminary evidence that an offspring polygenic risk score for major depressive disorder (PRS-MDD), based on European ancestry, interacts with prenatal maternal depressive symptoms (GxE) on neonatal right amygdalar (US and Asian cohort) and hippocampal volumes (Asian cohort). However, to date, this GxE interplay has only been addressed by one study and is yet unknown for a European ancestry sample. We investigated in 105 Finnish mother-infant dyads (44 female, 11-54 days old) how offspring PRS-MDD interacts with prenatal maternal depressive symptoms (Edinburgh Postnatal Depression Scale, gestational weeks 14, 24, 34) on infant amygdalar and hippocampal volumes. We found a GxE effect on right amygdalar volumes, significant in the main analysis, but nonsignificant after multiple comparison correction and some of the control analyses, whose direction paralleled the US cohort findings. Additional exploratory analyses suggested a sex-specific GxE effect on right hippocampal volumes. Our study is the first to provide support, though statistically weak, for an interplay of offspring PRS-MDD and prenatal maternal depressive symptoms on infant limbic brain volumes in a cohort matched to the PRS-MDD discovery sample.
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