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Published on: December 9, 2013
Consequences of oxygen deprivation on myelination and sex-dependent alterations
Rafael Bandeira Fabres1, Débora Sterzeck Cardoso2, Brian Aranibar Aragón3
1Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, Porto Alegre 90035-003, Brazil.
Insights
Neonatal oxygen deprivation causes white matter injury and neurodevelopmental issues. This review explores how sexual dimorphism affects neuroinflammation and oligodendrocyte injury following oxygen deprivation in newborns.
Area of Science:
- Neuroscience
- Developmental Biology
- Neonatal Medicine
Background:
- Oxygen deprivation is a major cause of newborn mortality and morbidity, particularly in preterm infants.
- White matter injury, impacting oligodendrocytes and myelination, is a key feature leading to long-term cognitive and motor deficits.
- Neuroinflammation and apoptotic pathways activated by oxygen deprivation may be influenced by sexual dimorphism.
Purpose of the Study:
- To review recent research on the impact of sexual dimorphism on neuroinflammation and white matter injury after neonatal oxygen deprivation.
- To provide an overview of oligodendrocyte lineage development and myelination.
- To examine the effects of oxygen deprivation and neuroinflammation on oligodendrocytes in neurodevelopmental disorders.
Main Methods:
- Literature review of recent studies.
- Analysis of oligodendrocyte lineage development and myelination processes.
- Investigation of neuroinflammation and apoptotic pathways in the context of neonatal oxygen deprivation and sexual dimorphism.
Main Results:
- Oxygen deprivation significantly impacts white matter integrity and oligodendrocyte function.
- Neuroinflammation plays a critical role in the pathogenesis of white matter injury.
- Emerging evidence suggests sexual dimorphism influences the response to oxygen deprivation, affecting neuroinflammation and oligodendrocyte injury.
Conclusions:
- Oligodendrocytes and myelination are crucial targets for therapeutic interventions following neonatal oxygen deprivation.
- Understanding sexual dimorphism in neuroinflammation and white matter injury is essential for developing targeted treatments.
- Further research is needed to elucidate the mechanisms underlying sexual dimorphism in neonatal hypoxic-ischemic brain injury.
Abstract:
Oxygen deprivation is one of the main causes of morbidity and mortality in newborns, occurring with a higher prevalence in preterm infants, reaching 20 % to 50 % mortality in newborns in the perinatal period. When they survive, 25 % exhibit neuropsychological pathologies, such as learning difficulties, epilepsy, and cerebral palsy. White matter injury is one of the main features found in oxygen deprivation injury, which can lead to long-term functional impairments, including cognitive delay and motor deficits. The myelin sheath accounts for much of the white matter in the brain by surrounding axons and enabling the efficient conduction of action potentials. Mature oligodendrocytes, which synthesize and maintain myelination, also comprise a significant proportion of the brain's white matter. In recent years, oligodendrocytes and the myelination process have become potential therapeutic targets to minimize the effects of oxygen deprivation on the central nervous system. Moreover, evidence indicate that neuroinflammation and apoptotic pathways activated during oxygen deprivation may be influenced by sexual dimorphism. To summarize the most recent research about the impact of sexual dimorphism on the neuroinflammatory state and white matter injury after oxygen deprivation, this review presents an overview of the oligodendrocyte lineage development and myelination, the impact of oxygen deprivation and neuroinflammation on oligodendrocytes in neurodevelopmental disorders, and recent reports about sexual dimorphism regarding the neuroinflammation and white matter injury after neonatal oxygen deprivation.
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