Yoko Nomura1,2,3,4, Rosalind M John5, Anna Bugge Janssen5, Charles Davey6, Jackie Finik7,6, Jessica Buthmann7,8, Vivette Glover9, Luca Lambertini10,11. 1. Department of Psychology, Queens College, the City University of New York, 65-30 Kissena Blvd, Flushing, NY, 11367, USA. yoko.nomura@qc.cuny.edu. 2. Graduate Center, the City University of New York, Flushing, USA. yoko.nomura@qc.cuny.edu. 3. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, USA. yoko.nomura@qc.cuny.edu. 4. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, USA. yoko.nomura@qc.cuny.edu. 5. Cardiff School of Biosciences, Cardiff University, Cardiff, UK. 6. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, USA. 7. Department of Psychology, Queens College, the City University of New York, 65-30 Kissena Blvd, Flushing, NY, 11367, USA. 8. Graduate Center, the City University of New York, Flushing, USA. 9. Imperial Collage of London, London, UK. 10. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, USA. 11. Department of Obstetrics, Gynecology and Reproductive Science, Icahn School of Medicine at Mount Sinai, New York, USA.
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.
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.
Authors: Ertugrul M Ozbudak; Mukund Thattai; Iren Kurtser; Alan D Grossman; Alexander van Oudenaarden Journal: Nat Genet Date: 2002-04-22 Impact factor: 38.330
Authors: Kathrine Skak Madsen; Terry L Jernigan; Pernille Iversen; Vibe G Frokjaer; Erik Lykke Mortensen; Gitte M Knudsen; William F C Baaré Journal: Psychiatry Res Date: 2012-01-30 Impact factor: 3.222
Authors: Daniel A Enquobahrie; Margaret Meller; Kenneth Rice; Bruce M Psaty; David S Siscovick; Michelle A Williams Journal: Am J Obstet Gynecol Date: 2008-06-04 Impact factor: 8.661
Authors: Forgive Avorgbedor; Susan Silva; Elizabeth Merwin; James A Blumenthal; Diane Holditch-Davis Journal: J Obstet Gynecol Neonatal Nurs Date: 2018-11-29
Authors: Gillian M Maher; Gerard W O'Keeffe; Patricia M Kearney; Louise C Kenny; Timothy G Dinan; Molly Mattsson; Ali S Khashan Journal: JAMA Psychiatry Date: 2018-08-01 Impact factor: 21.596
Authors: G I McNamara; H D J Creeth; D J Harrison; K E Tansey; R M Andrews; A R Isles; R M John Journal: Hum Mol Genet Date: 2018-02-01 Impact factor: 6.150
Authors: Gillian M Maher; Gerard W O'Keeffe; Louise C Kenny; Patricia M Kearney; Ted G Dinan; Ali S Khashan Journal: BMJ Open Date: 2017-10-05 Impact factor: 2.692