Obehioya Irumudomon
Institution: Case Western Reserve
The incidence of preterm births continues rise. Many of these children have chronic neurological deficits due to brain injury they suffered in utero from a combination of infection and placental insufficiency. We hypothesize that exogenous erythropoietin (EPO) will mitigate neural cell death induced after prenatal brain injury.
EPO is an important growth factor during CNS development, and is known to suppress inflammatory responses and act as a neuroprotectant through multiple signaling pathways. A rat model that combines both prenatal inflammation and hypoxia-ischemia will be used to investigate how EPO minimizes cell death and the inflammatory response after prenatal brain injury. The research will begin to elucidate the mechanisms of EPO signaling after prenatal insults and reveal a potential mechanism for a novel drug intervention for these infants. The implications of this mechanism of neuroprotection may also provide insights into treatment of other forms of CNS injury with EPO. |