3141 Chestnut Street
B.S., Biomedical Engineering, University of Virginia, 2008
My project concerns Traumatic Brain Injury, and we use an in vitro model of cell injury to replicate morphological effects that have been observed after in vivo injury. At the cellular level, there are both primary and secondary effects of mechanical trauma to the neurons. Mechanical trauma causes primary membrane damage that leads to secondary degradation of the cytoskeleton and impaired axonal transport and initiates a cascade of chemical signals that lead to further axonal disconnection and ultimately to cell death. Using a block copolymer called Poloxamer 188(P188), we can treat this initial membrane damage, thereby saving the cell. But is the cell fully functional? What else happens after injury? The membrane resealing properties of P188 provide both an opportunity for assessing the role of membrane damage in TBI as well as a potential therapeutic approach after injury.
Currently, I am attempting to better undertand the effect of injury on axonal transport by observing the movement of mitochondria before and after injury.