Vulnerability of premyelinating oligodendrocytes to white-matter damage in neonatal brain injury

Xiao Bo Liu, Yan Shen, Jennifer M. Plane, Wenbin Deng

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


Premature birth is a significant economic and public health burden, and its incidence is rising. Periventricular leukomalacia (PVL) is the predominant form of brain injury in premature infants and the leading cause of cerebral palsy. PVL is characterized by selective white-matter damage with prominent oligodendroglial injury. The maturation-dependent vulnerability of developing and premyelinating oligodendrocytes to excitotoxic, oxidative, and inflammatory forms of injury is a major factor in the pathogenesis of PVL. Recent studies using mouse models of PVL reveal that synapses between axons and developing oligodendrocytes are quickly and profoundly damaged in immature white matter. Axon-glia synapses are highly vulnerable to white-matter injury in the developing brain, and the loss of synapses between axons and premyelinating oligodendrocytes occurs before any cellular loss in the immature white matter. Microglial activation and astrogliosis play important roles in triggering white-matter injury. Impairment of white-matter development and function in the neonatal period contributes critically to functional and behavioral deficits. Preservation of the integrity of the white matter is likely key in the treatment of PVL and subsequent neurological consequences and disabilities.

Original languageEnglish (US)
Pages (from-to)229-238
Number of pages10
JournalNeuroscience Bulletin
Issue number2
StatePublished - Apr 2013


  • myelin
  • neonatal brain injury
  • oligodendrocyte
  • periventricular leukomalacia
  • prematurity
  • white matter

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)


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