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Blocked, delayed, or obstructed: What causes poor white matter development in intrauterine growth restricted infants?
Mary Tolcos1, Steven Petratos2, Jonathan J Hirst3
1School of Health and Biomedical Sciences, RMIT University, Bundoora, Victoria, 3083, Australia.
Insights
Intrauterine growth restriction (IUGR) impairs white matter development in newborns, leading to neurodevelopmental issues. This review explores causes and promising therapies to promote oligodendrocyte maturation and repair myelin deficits.
Area of Science:
- Neonatology
- Neuroscience
- Developmental Biology
Background:
- Intrauterine growth restriction (IUGR) is a major cause of neonatal morbidity, second only to preterm birth.
- IUGR is a significant risk factor for cerebral palsy, with white matter development issues being a key concern.
- Current understanding of impaired myelination largely stems from adult demyelinating diseases or preterm brain injury, with less focus on IUGR.
Purpose of the Study:
- To review current understanding of poor white matter development in IUGR neonates.
- To discuss the mechanisms underlying oligodendrocyte development and myelin formation in IUGR.
- To explore novel therapeutic interventions for promoting oligodendrocyte maturation and repairing myelination deficits.
Main Methods:
- This is a review article, synthesizing existing research and literature.
- It examines mechanisms of oligodendrocyte maturation and myelination.
- It discusses potential therapeutic strategies based on current scientific evidence.
Main Results:
- IUGR is associated with hypomyelination in the central nervous system of neonates.
- Evidence suggests a delay or blockade in oligodendrocyte maturation contributes to reduced myelination in IUGR infants.
- Understanding these mechanisms is crucial for developing effective treatments.
Conclusions:
- Poor white matter development in IUGR is a significant, untreated problem requiring novel therapeutic approaches.
- Targeting oligodendrocyte maturation holds promise for repairing myelination deficits and preventing long-term neurodevelopmental abnormalities.
- Further research into IUGR-specific mechanisms is needed to guide effective interventions.
Abstract:
Poor white matter development in intrauterine growth restricted (IUGR) babies remains a major, untreated problem in neonatology. New therapies, guided by an understanding of the mechanisms that underlie normal and abnormal oligodendrocyte development and myelin formation, are required. Much of our knowledge of the mechanisms that underlie impaired myelination come from studies in adult demyelinating disease, preterm brain injury, or experimental models of hypoxia-ischemia. However, relatively less is known for IUGR which is surprising because IUGR is a leading cause of perinatal mortality and morbidity, second only to premature birth. IUGR is also a significant risk factor for the later development of cerebral palsy, and is a greater risk compared to some of the more traditionally researched antecedents - asphyxia and inflammation. Recent evidence suggests that the white matter injury and reduced myelination in the brains of some preterm babies is due to impaired maturation of oligodendrocytes thereby resulting in the reduced capacity to synthesize myelin. Therefore, it is not surprising that the hypomyelination observable in the central nervous system of IUGR infants has similarly lead to investigations identifying a delay or blockade in the progress of maturation of oligodendrocytes in these infants. This review will discuss current ideas thought to account for the poor myelination often present in the neonate's brain following IUGR, and discuss novel interventions that are promising as treatments that promote oligodendrocyte maturation, and thereby repair the myelination deficits that otherwise persist into infancy and childhood and lead to neurodevelopmental abnormalities.