Neuronal damage accompanies perinatal white-matter damage.
Extremely low-gestational-age newborns have a prominently increased risk of brain dysfunctions attributed to white-matter damage, which is thought to result from the vulnerability of the oligodendrocyte. This white-matter damage now appears to be accompanied by cerebral-cortex and deep-gray-matter abnormalities, including excess apoptosis without replacement and the impairment of surviving neurons and resulting interference with synaptogenesis and connectivity. Recent advances in corticogenesis suggest that neurons migrate from the germinative zones through the white matter to the cortex when the white matter is most vulnerable and perhaps is being injured. Advances in developmental neuroscience also suggest that the excitotoxic and inflammatory processes that probably contribute to white-matter damage are also able to damage developing neurons. Together, these advances support the untested hypothesis that white-matter damage in the preterm newborn is accompanied by the death of neurons as they migrate through the dangerous minefield of white matter undergoing injury.
Leviton
Alan
A
Department of Neurology, Children's Hospital Boston, Boston, MA, USA. alan.leviton@childrens.harvard.edu
Gressens
Pierre
P
D000818:Animals; D001925:Brain Damage, Chronic / Q000473:pathology*; D002540:Cerebral Cortex / Q000254:growth & development; D018846:Excitatory Amino Acids / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000502:physiology*; D007249:Inflammation / Q000473:pathology; D009474:Neurons / Q000473:pathology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D018846:Excitatory Amino Acids; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid