Dr. Pelin Cengiz’s research focuses on finding a novel therapy for neonatal encephalopathy subsequent to hypoxia ischemia (HI). She uses the experimental (Vannucci-Rice) mouse model of hypoxia ischemia (HI) to study the sexually differentiated role of neurotrophin signaling in the neonatal hippocampus post-HI. The neurotrophin receptor, tyrosine kinase B (TrkB), plays an important role in neuroprotection and improving the long-term functional recovery following cerebral ischemia by increasing neuronal survival. She has shown that administration of 7,8 dihydroxyflavone (7,8-DHF; potent and selective TrkB agonist) increases TrkB phosphorylation and hippocampal neuronal survival following HI in female, but not in male newborn mice. This female-specific responsiveness to TrkB agonist therapy mimics improved outcomes observed clinically in female newborn humans post-HI. Her studies focus on the cellular mechanisms of the female-specific responsiveness to TrkB agonist and their roles in improving long-term neurological and functional outcome post-HI. An improved understanding of the cellular mechanisms that underlie sex-specific neurotrophin responses will identify new avenues for developing novel therapeutics for neonates and children suffering from brain injury.