Ischemic injury following vascular occlusion is often dictated by pre-existing pial collateral or "by-pass" vessels. Our overall goal is to improve collateral remodeling and to understand how this influences the microenvironment in which neurons repair themselves.
There is a paucity of data that limits our understanding of innate immune regulation across the age spectrum following TBI. Exploiting the pro-resolving phenotype of young innate immune cells may provide a novel restorative intervention aimed at improving TBI outcomes and reveal novel targets for drug discovery.
Limited information exists pertaining to the physiological relevance of innate immune regulation and the key players driving their phenotypic response following TBI. Completion of these studies will advance our understanding of how peripheral-derived monocyte/macrophages dictates neurovascular injury and recovery in the pathophysiology of TBI.
Promoting vascular remodeling has emerged as a potential therapeutic approach for neurorestorative therapy. New insights into the regulation of cerebral vascular trauma will aid our understanding of the impact of TBI on cerebral blood flow loss, which potentiates neuronal cell loss resulting in motor and cognitive deficits in models of brain injury.
Virginia Tech is launching a $2.6 million study to determine if traumatic brain injuries can cause changes within the brain that lead to epilepsy. Funded by the nonprofit Citizens United for Research in Epilepsy (CURE) and the U.S. Department of Defense, the three-year study seeks to identify the root causes behind why a person may develop epilepsy after he or she has suffered brain trauma, including sports-related concussion and focal contusion injuries.