Citation

Deng W. Nat. Rev. Neurol. 2010; 6(6): 328-336.

Affiliation

Department of Cell Biology and Human Anatomy, Institute for Pediatric Regenerative Medicine, School of Medicine, University of California Davis, 2425 Stockton Boulevard, Sacramento, CA 95817, USA. wbdeng@ucdavis.edu.

Copyright

(Copyright © 2010, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1038/nrneurol.2010.53

PMID

20479779

Abstract

Owing to improved survival rates of premature newborns, the number of very low birth weight infants is rising. Preterm infants display a greater propensity for brain injury caused by hypoxic or ischemic events, infection and/or inflammation that results in prominent white matter injury (WMI) than infants carried to full term. The intrinsic vulnerability of developing oligodendroglia to excitotoxic, oxidative and inflammatory forms of injury is a major factor in the pathogenesis of this condition. Furthermore, activated microglia and astrogliosis are critically involved in triggering WMI. Currently, no specific treatment is available for this kind of injury. Injury to the premature brain can substantially influence brain development and lead to disability. Impairment of the main motor pathways, such as the corticospinal tract, in the perinatal period contributes substantially to clinical outcome. Advanced neuroimaging techniques have led to greater understanding of the nature of both white and gray matter injury in preterm infants. Further research is warranted to examine the translational potential of preclinical therapeutic strategies for controlling such injury and preserving the integrity of motor pathways in preterm infants.

Language: en