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Molecular and biochemical mechanisms of perinatal brain injury
1Department of Neurology, University California San Francisco, 521 Parnassus Ave, San Francisco, CA 94143-0114, USA.
Insights
Hypoxic-ischemic brain injury impacts infant health, causing developmental issues. This review explores the molecular mechanisms behind neonatal brain injury and potential therapeutic targets.
Area of Science:
- Neuroscience
- Developmental Biology
- Perinatal Medicine
Background:
- Hypoxic-ischemic (HI) injury is a leading cause of infant neurological disability.
- The developing brain's vulnerability to HI injury is influenced by developmental stage and blood flow regulation.
Purpose of the Study:
- To review the molecular and biochemical mechanisms of acute brain injury in neonates following hypoxic-ischemic events.
- To examine the role of intracellular homeostasis, neurotransmitters, free radicals, and gene expression in neonatal brain injury.
Main Methods:
- Review of experimental rodent and murine models of hypoxic-ischemic and ischemic injury.
- Analysis of molecular and biochemical pathways involved in acute neonatal brain damage.
Main Results:
- HI injury disrupts intracellular homeostasis and involves glutamate excitotoxicity.
- Free radicals and transitional ions contribute to oxidative stress and cell damage.
- Gene expression plays a critical role in modulating cell death and survival pathways.
Conclusions:
- Understanding the molecular mechanisms of neonatal HI brain injury is crucial for developing effective treatments.
- Targeting specific pathways, such as glutamate receptors and oxidative stress, may offer therapeutic benefits.
Abstract:
Hypoxic-ischemic injury to the prenatal and perinatal brain is a major contributor to morbidity and mortality to infants, often leading to mental retardation, seizures, and cerebral palsy. The susceptibility of the immature CNS to hypoxia-ischemia is largely dependent on the temporal and regional status of critical developmental processes, as well as on the regulation of cerebral blood flow and metabolism. The molecular and biochemical mechanisms of acute injury to the neonatal brain in experimental rodent and murine models of hypoxic-ischemic and ischemic injury, including disturbances of intracellular homeostasis, role of glutamate receptors, free radicals and transitional ions, as well as the modifying role of gene expression to cell death/survival will be reviewed in this chapter.