UK NETT Clinical Hub Site: BIO-ProTECT

Grants and Contracts Details


Traumatic Brain Injury (TBI) is the leading cause of death and disability among young adults in the US and worldwide.1-2 The pathophysiology of acute TBI is characterized by a cascade of cellular events set in motion by the initial injury, and ultimately leading to cerebral edema, cellular disruption and death. Tissue breakdown in TBI results in the release of structural proteins into the bloodstream, including S100B protein (S100B), glial fibrillary acidic protein (GFAP), and Ubiquitin C-Hydrolase L1 (UCH-L1). Cellular necrosis and apoptosis are reflected in the proteolysis of áII-Spectrin into breakdown products (SBDP). Serum blood levels of S100B, GFAP, UCH-L1 and SBDP150 may correlate with the extent of brain injury, which, in turn may influence the prognosis. If so, these proteins could serve as useful biomarkers for the severity of the injury, the patient’s prognosis, and could potentially be used to guide treatment. Preliminary data from our group suggest that the serum levels of S100B, GFAP, UCH-L1 and SBDP150 may more accurately predict the extent of injury than the Glasgow Coma Scale (GCS) and computed tomography (CT). However, none of these potential biomarkers have been sufficiently validated to be used clinically. We propose to provide such validation data, using a large group of TBI patients who are enrolled in an ongoing phase III trial of progesterone effects in acute TBI, the ProTECT III trial.
Effective start/end date5/1/114/30/14


  • University of Michigan


Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.