Protective astrogenesis from the SVZ niche after injury is controlled by Notch modulator Thbs4.

As a neonatologist, my research interests revolve around improving the survival and quality of life of high-risk neonates cared for in Neonatal Intensive Care Units. My primary interest is perinatal brain injuries impacting both full-term infants and those born prematurely.  One of the most common forms of perinatal brain injury involves damage to white matter (myelin). My laboratory has developed models of perinatal brain injury to investigate how the endogenous neural stem cell responds to myelin injury. Our hope is to develop innovative strategies to successfully redirect stem cells into the oligodendrocyte lineage and promote myelination after injury.  In order to successfully restore myelination after injury, we want to better understand the molecular mechanisms governing 2 important aspects of myelin development. 

First, we must understand the molecular signals that drive neural stem cells to differentiate into oligodendrocytes (oligodendrogenesis) and how brain injury impacts this process. This interest has led my laboratory to investigate intracellular and extracellular changes that occur in the neural stem cell niche following injuries that lead to white matter damage. 

Secondly, after stem cell commitment to the oligodendrocyte lineage has occurred, we must understand the ongoing signals from the neural environment that influence oligodendrocyte maturation. For this work, my laboratory has developed an innovative technology to remotely control ion channels non-invasively using magnetic fields. Using this technology, we are developing strategies to alter the activity of targeted neural circuits both in utero as well as postnatally to understand the impact of altered activity on myelin maturation. Members of my laboratory are also currently using this technology to understand how altered temperature-gated channel activity in utero may contribute to birth defects associated with maternal fevers. 

We have successfully developed various rodent models of brain and spinal cord injuries in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma, subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression injury. We also established cardiac arrest and hemorrhagic shock models for studying multiple organ dysfunction.  Our current studies focus on two projects. One is to examine the efficacy of catalytic antioxidant in treating cerebral ischemia and the other is to examine the efficacy of post-conditioning on outcome of subarachnoid hemorrhage induced cognitive dysfunction.