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Neurobiology of premature brain injury

Nature Neuroscience volume 17, pages 341346 (2014) | Download Citation

Abstract

Every year in the United States, an estimated 500,000 babies are born preterm (before 37 completed weeks of gestation), and this number is rising, along with the recognition of brain injuries due to preterm delivery. A common underlying pathogenesis appears to be perinatal hypoxia induced by immature lung development, which causes injury to vulnerable neurons and glia. Abnormal growth and maturation of susceptible cell types, particularly neurons and oligodendrocytes, in preterm babies with very low birth weight is associated with decreased cerebral and cerebellar volumes and increases in cerebral ventricular size. Here we reconcile these observations with recent studies using models of perinatal hypoxia that show perturbations in the maturation and function of interneurons, oligodendrocytes and astroglia. Together, these findings suggest that the global mechanism by which perinatal hypoxia alters development is through a delay in maturation of affected cell types, including astroglia, oligodendroglia and neurons.

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Acknowledgements

This research has been supported by the US National Institutes of Health NINDS (P01 NS062686 and R01 NS060750 to F.M.V. and R01NS045702 to V.G.), NICHD (P30HD040677 to V.G.) and NIA (R21 AG034495 to FMV), and by grants from the Brain and Behavior Research Foundation (F.M.V.), the state of Connecticut (F.M.V.), Women's Health Research at Yale (F.M.V.) and the Cerebral Palsy International Research Foundation (V.G.). N.S. is recipient of a Canadian Institute of Health Research fellowship. J.S. is the recipient of K08NS073793 (NINDS). We are particularly grateful to L. Ment for support and discussion. We thank J. Ritter for help with figures.

Author information

Affiliations

  1. Child Study Center, Yale University, New Haven, Connecticut, USA.

    • Flora M Vaccarino
  2. Program in Neurodevelopment and Regeneration, Yale University, New Haven, Connecticut, USA.

    • Natalina Salmaso
    •  & Flora M Vaccarino
  3. Center for Neuroscience Research, Children's National Medical Center, Washington, DC, USA.

    • Beata Jablonska
    • , Joseph Scafidi
    •  & Vittorio Gallo
  4. Kavli Institute for Neuroscience, Yale University, New Haven, Connecticut, USA.

    • Flora M Vaccarino
  5. Department of Neurobiology, Yale University, New Haven, Connecticut, USA.

    • Flora M Vaccarino

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Competing interests

The authors declare no competing financial interests.

Corresponding authors

Correspondence to Flora M Vaccarino or Vittorio Gallo.

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DOI

https://doi.org/10.1038/nn.3604

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