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Review

Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key

1
Department of Pediatrics, Maastricht University Medical Center, 6202 AZ Maastricht, The Netherlands
2
School for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands
3
School for Mental Health and Neuroscience (MHeNS), Maastricht University, 6229 ER Maastricht, The Netherlands
4
Department of Pediatric Neurology, Maastricht University Medical Center, 6202 AZ Maastricht, The Netherlands
5
Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Private bag 92019, Auckland 1023, New Zealand
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2020, 9(8), 1871; https://doi.org/10.3390/cells9081871
Received: 8 June 2020 / Revised: 31 July 2020 / Accepted: 5 August 2020 / Published: 10 August 2020
With a worldwide incidence of 15 million cases, preterm birth is a major contributor to neonatal mortality and morbidity, and concomitant social and economic burden Preterm infants are predisposed to life-long neurological disorders due to the immaturity of the brain. The risks are inversely proportional to maturity at birth. In the majority of extremely preterm infants (<28 weeks’ gestation), perinatal brain injury is associated with exposure to multiple inflammatory perinatal triggers that include antenatal infection (i.e., chorioamnionitis), hypoxia-ischemia, and various postnatal injurious triggers (i.e., oxidative stress, sepsis, mechanical ventilation, hemodynamic instability). These perinatal insults cause a self-perpetuating cascade of peripheral and cerebral inflammation that plays a critical role in the etiology of diffuse white and grey matter injuries that underlies a spectrum of connectivity deficits in survivors from extremely preterm birth. This review focuses on chorioamnionitis and hypoxia-ischemia, which are two important antenatal risk factors for preterm brain injury, and highlights the latest insights on its pathophysiology, potential treatment, and future perspectives to narrow the translational gap between preclinical research and clinical applications. View Full-Text
Keywords: preterm brain injury; hypoxia-ischemia; chorioamnionitis; timing; therapeutic hypothermia; stem cells; annexin A1; erythropoietin; biomarkers preterm brain injury; hypoxia-ischemia; chorioamnionitis; timing; therapeutic hypothermia; stem cells; annexin A1; erythropoietin; biomarkers
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MDPI and ACS Style

Ophelders, D.R.M.G.; Gussenhoven, R.; Klein, L.; Jellema, R.K.; Westerlaken, R.J.J.; Hütten, M.C.; Vermeulen, J.; Wassink, G.; Gunn, A.J.; Wolfs, T.G.A.M. Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key. Cells 2020, 9, 1871. https://doi.org/10.3390/cells9081871

AMA Style

Ophelders DRMG, Gussenhoven R, Klein L, Jellema RK, Westerlaken RJJ, Hütten MC, Vermeulen J, Wassink G, Gunn AJ, Wolfs TGAM. Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key. Cells. 2020; 9(8):1871. https://doi.org/10.3390/cells9081871

Chicago/Turabian Style

Ophelders, Daan R.M.G., Ruth Gussenhoven, Luise Klein, Reint K. Jellema, Rob J.J. Westerlaken, Matthias C. Hütten, Jeroen Vermeulen, Guido Wassink, Alistair J. Gunn, and Tim G.A.M. Wolfs. 2020. "Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key" Cells 9, no. 8: 1871. https://doi.org/10.3390/cells9081871

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