Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes

Nomura, Yoko, John, Rosalind Margaret ORCID: https://orcid.org/0000-0002-3827-7617, Bugge Janssen, Anna, Davey, Charles, Finik, Jackie, Buthmann, Jessica, Glover, Vivette and Lambertini, Luca 2017. Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes. Archives of Gynecology and Obstetrics 295 (6) , pp. 1319-1329. 10.1007/s00404-017-4347-3

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Abstract

Purpose Preeclampsia is known to be a leading cause of mortality and morbidity among mothers and their infants. Approximately 3–8% of all pregnancies in the US are complicated by preeclampsia and another 5–7% by hypertensive symptoms. However, less is known about its long-term influence on infant neurobehavioral development. The current review attempts to demonstrate new evidence for imprinting gene dysregulation caused by hypertension, which may explain the link between maternal preeclampsia and neurocognitive dysregulation in offspring. Method Pub Med and Web of Science databases were searched using the terms “preeclampsia,” “gestational hypertension,” “imprinting genes,” “imprinting dysregulation,” and “epigenetic modification,” in order to review the evidence demonstrating associations between preeclampsia and suboptimal child neurodevelopment, and suggest dysregulation of placental genomic imprinting as a potential underlying mechanism. Results The high mortality and morbidity among mothers and fetuses due to preeclampsia is well known, but there is little research on the long-term biological consequences of preeclampsia and resulting hypoxia on the fetal/child neurodevelopment. In the past decade, accumulating evidence from studies that transcend disciplinary boundaries have begun to show that imprinted genes expressed in the placenta might hold clues for a link between preeclampsia and impaired cognitive neurodevelopment. A sudden onset of maternal hypertension detected by the placenta may result in misguided biological programming of the fetus via changes in the epigenome, resulting in suboptimal infant development. Conclusion Furthering our understanding of the molecular and cellular mechanisms through which neurodevelopmental trajectories of the fetus/infant are affected by preeclampsia and hypertension will represent an important first step toward preventing adverse neurodevelopment in infants.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Uncontrolled Keywords:	Genomic imprinting Placenta Epigenetics Preeclampsia Neurobehavioral development
Publisher:	Springer
ISSN:	0932-0067
Date of First Compliant Deposit:	2 May 2017
Date of Acceptance:	7 March 2017
Last Modified:	19 Nov 2024 18:30
URI:	https://orca.cardiff.ac.uk/id/eprint/100238

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