Welcome to the Buckwalter Lab
Are in how inflammatory responses after brain injury affect neurological recovery. In the United States, there are 4 million people currently living with the effects of stroke, and another 4.3 million living with the effects of traumatic brain injury.
Of the people who have had a stroke, many are disabled to the degree that they cannot work, and a significant proportion are unable to walk, feed themselves, or communicate with their families the way they could prior to their stroke.
Despite this very high number of people who are suffering, there is a large knowledge gap regarding the mechanisms by which neurological recovery occurs, and not a single FDA-approved therapy available to help people recover. There is reason to think that such a therapy might be obtainable – we know that some people, especially younger ones, experience significant recovery after stroke.
Neural death resulting from an injury or stroke can be exacerbated by immune responses, which can damage neurons directly via neurotoxic cytokines or indirectly via brain swelling within the closed space of the skull.
Our goal is thus to understand how inflammatory responses contribute to brain damage after stroke and how they influence recovery. In particular, we are interested in inflammatory signaling of glial cells in both the central nervous system and the periphery in models of stroke and infection.