Dysmaturation of Premature Brain: Importance, Cellular Mechanisms, and Potential Interventions

Joseph J Volpe1

  • 1Department of Neurology, Harvard Medical School, Boston, Massachusetts; Department of Pediatric Newborn Medicine, Harvard Medical School, Boston, Massachusetts.

Pediatric Neurology
|April 13, 2019
PubMed

Insights

Preterm birth can lead to brain dysmaturation and neurodevelopmental disabilities. Interventions targeting cellular mechanisms, nutrition, and environmental enrichment show promise for preventing or improving outcomes in premature infants.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Neonatology

Background:

  • Preterm birth (less than 32 weeks' gestation) is common and linked to significant neurodevelopmental disabilities, particularly cognitive deficits.
  • The underlying cause is brain dysmaturation, often following initial injury like cerebral white matter injury.
  • This dysmaturation affects critical developmental events in both white and gray matter during the premature period.

Purpose of the Study:

  • To review the developmental events and dysmaturation processes occurring in premature infants' brains.
  • To emphasize the cellular mechanisms, particularly involving preoligodendrocytes, microglia, and astrocytes, in brain dysmaturation.
  • To explore potential neurorestorative interventions for preventing or ameliorating these developmental disturbances.

Main Methods:

  • Review of existing literature on brain development in preterm infants.
  • Focus on cellular mechanisms of dysmaturation, including glial cell roles (microglia, astrocytes) and oligodendrocyte precursor cells.
  • Analysis of potential interventions: pharmacological (e.g., erythropoietin), nutritional (e.g., fatty acids, iron, zinc), and experiential (e.g., sensory input, stress reduction).

Main Results:

  • Brain dysmaturation in preterm infants involves complex cellular mechanisms.
  • Activated microglia and reactive astrocytes play a central role in the dysmaturation process.
  • The extended timeframe of these cellular mechanisms suggests a window for therapeutic intervention.

Conclusions:

  • Neurorestorative interventions targeting cellular, nutritional, and experiential factors are feasible.
  • Pharmacological agents like erythropoietin show potential.
  • Optimizing nutrition and providing enriched sensory and environmental experiences are crucial for enhancing brain development in premature infants.

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