Hypoxia-ischemia (HI) and associated encephalopathy (HIE) are among the leading causes of significant mortality and long-term neurological morbidity during the perinatal period with an incidence of 2-4/1000 full term and 5-6/1000 premature births. Neonates exposed to HI injury can have poor neurological and behavioral outcomes including increased risks and incidences of learning deficits and disabilities due to the diffuse nature of the insults. Consequently, developmental disabilities place a huge burden on society (estimated lifetime costs per person: ~1 million dollars), emphasizing the urgent need for identifying mechanism(s) underlying HIE and improved prevention/treatment strategies to reduce perinatal brain damage.
Although recent work has revealed numerous mechanisms predisposing to HI injury, these mechanisms including neuroinflammation, cell death, mitochondrial dysfunction, oxidative stress, and excitotoxicity are complex and new therapeutical target molecules such as pro-inflammatory cytokines and DAMPs are continually being identified. There is now a strong therapeutic basis to treat full-term infants with moderate HIE with hypothermia, but this therapy is only supportive and cannot be used to treat preterm infants and full-term infants with HIE when started within 6 hours of birth. Xenon or erythropoietin (EPO) are two of the most attractive adjunct therapies. However, treatment with xenon or EPO alone or combined treatment with hypothermia does not improve functional outcomes in infants with severe HIE and extremely premature infants. Hence, there is a critical need to identify the additional mechanism(s) underlying HI and HIE to develop novel neuroprotective approaches.
This Research Topic aims to continue investigating the additional molecular and cellular mechanism(s) underlying HI and HIE using in vitro and in vivo models, bioinformatics analyses, MRI, and any other research tools. Also, this Research Topic focuses on exploring potential therapeutic strategies and their neuroprotective outcomes including hypothermia, stem cells, anti-inflammatory responses, and immunomodulation.
• Pathogenesis & neuroepigenetics
• Mechanisms: neuroinflammation, cell death, mitochondrial dysfunction, oxidative stress, excitotoxicity, blood-brain barrier damage, extracellular matrix dysfunction, and neuro-glia cell interactions
• Therapeutic strategies: hypothermia, stem cell therapy, anti-inflammation and cell death, and immunomodulation
• Molecular targets and biomarkers
• Research tools: in vivo animal and in vitro cell models, and bioinformatics and imaging tools.
• Behavioral outcomes.
Hypoxia-ischemia (HI) and associated encephalopathy (HIE) are among the leading causes of significant mortality and long-term neurological morbidity during the perinatal period with an incidence of 2-4/1000 full term and 5-6/1000 premature births. Neonates exposed to HI injury can have poor neurological and behavioral outcomes including increased risks and incidences of learning deficits and disabilities due to the diffuse nature of the insults. Consequently, developmental disabilities place a huge burden on society (estimated lifetime costs per person: ~1 million dollars), emphasizing the urgent need for identifying mechanism(s) underlying HIE and improved prevention/treatment strategies to reduce perinatal brain damage.
Although recent work has revealed numerous mechanisms predisposing to HI injury, these mechanisms including neuroinflammation, cell death, mitochondrial dysfunction, oxidative stress, and excitotoxicity are complex and new therapeutical target molecules such as pro-inflammatory cytokines and DAMPs are continually being identified. There is now a strong therapeutic basis to treat full-term infants with moderate HIE with hypothermia, but this therapy is only supportive and cannot be used to treat preterm infants and full-term infants with HIE when started within 6 hours of birth. Xenon or erythropoietin (EPO) are two of the most attractive adjunct therapies. However, treatment with xenon or EPO alone or combined treatment with hypothermia does not improve functional outcomes in infants with severe HIE and extremely premature infants. Hence, there is a critical need to identify the additional mechanism(s) underlying HI and HIE to develop novel neuroprotective approaches.
This Research Topic aims to continue investigating the additional molecular and cellular mechanism(s) underlying HI and HIE using in vitro and in vivo models, bioinformatics analyses, MRI, and any other research tools. Also, this Research Topic focuses on exploring potential therapeutic strategies and their neuroprotective outcomes including hypothermia, stem cells, anti-inflammatory responses, and immunomodulation.
• Pathogenesis & neuroepigenetics
• Mechanisms: neuroinflammation, cell death, mitochondrial dysfunction, oxidative stress, excitotoxicity, blood-brain barrier damage, extracellular matrix dysfunction, and neuro-glia cell interactions
• Therapeutic strategies: hypothermia, stem cell therapy, anti-inflammation and cell death, and immunomodulation
• Molecular targets and biomarkers
• Research tools: in vivo animal and in vitro cell models, and bioinformatics and imaging tools.
• Behavioral outcomes.
