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|Location:||College of Medicine Room 1306|
|Event Host:||Helen Phipps, Ph.D. Candidate|
Numerous studies support the role of kallikreain 6 (Klk6) as a critical component to various neuroinflammatory diseases and demyelination. Rising Klk6 is characteristic of multiple sclerosis and spinal cord injury. Falling Klk6 is characteristic of Alzheimer's disease. However, Klk6 with respect to traumatic brain injury (TBI) is unknown. The secondary neuroinflammatory cascades in the acute phase (first 72h) of TBI are often the most devestating to patient outcome. This study aims to identify Klk6 as a novel neuroinflammatory biomarker implicated in the acute phase post-TBI and subsequently establishes abundance of Klk6 in brain and blood tissue as a function of time since TBI.
|Contact Name:||Daettia Butler|