4.6 Review

The role of inflammation in perinatal brain injury

Journal

NATURE REVIEWS NEUROLOGY
Volume 11, Issue 4, Pages 192-208

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/nrneurol.2015.13

Keywords

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Funding

  1. Leducq Foundation [DSRR_P34404]
  2. Wellcome Trust programme [WT094823MA]
  3. NIH [NS033997, 082330, RO1NS44025, NS76726, R21NS083425]
  4. Swedish Medical Research Council [VR2012-3500, VR2012-2992]
  5. ALF-LUA [ALFGBG432291, ALFGBG426401]
  6. European Union grant FP7 (Neurobid) [HEALTHF2-2009-241778]
  7. Swedish Brain Foundation [FO2013-095, FO2013-0035]
  8. Wilhelm & Martina Lundgren Foundation
  9. Frimurarna Barnhusdirektionen Foundation
  10. Byggmastare Olle Engkvist Foundation
  11. ERA-Net
  12. EU [VR 2014-7551]
  13. DHU PROTECT
  14. INSERM
  15. University Paris 7
  16. Fondation Graca de Monaco
  17. Fondation de Spoelberch
  18. MRC [G0802853] Funding Source: UKRI
  19. Medical Research Council [G0802853] Funding Source: researchfish

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Inflammation is increasingly recognized as being a critical contributor to both normal development and injury outcome in the immature brain. The focus of this Review is to highlight important differences in innate and adaptive immunity in immature versus adult brain, which support the notion that the consequences of inflammation will be entirely different depending on context and stage of CNS development. Perinatal brain injury can result from neonatal encephalopathy and perinatal arterial ischaemic stroke, usually at term, but also in preterm infants. Inflammation occurs before, during and after brain injury at term, and modulates vulnerability to and development of brain injury. Preterm birth, on the other hand, is often a result of exposure to inflammation at a very early developmental phase, which affects the brain not only during fetal life, but also over a protracted period of postnatal life in a neonatal intensive care setting, influencing critical phases of myelination and cortical plasticity. Neuroinflammation during the perinatal period can increase the risk of neurological and neuropsychiatric disease throughout childhood and adulthood, and is, therefore, of concern to the broader group of physicians who care for these individuals.

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