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Characterization of a Novel Model for Rotational Acceleration-induced Traumatic Brain Injury

Raegan Adams, Alan Umfress, James Bibb, Department of Surgery, University of Alabama at Birmingham, 1720 University Blvd, Birmingham, AL 35294

Millions of sports-related injuries occur annually in the U.S., causing a wide array of acute and chronic pathologies. During In these traumatic brain injuries (TBIs) the head undergoes rapid acceleration and deceleration, resulting in both linear and rotational forces that damage circuitry and impact brain function. While both linear and rotational forces can cause TBI, the brain is more sensitive to rotational motion, which can produce shearing forces that damage underlying deep subcortical structures of the brain such as the midbrain, amygdala, and hippocampal formation. Damage to these deeper structures, such as the hippocampus, underlie deficits in cognitive impairment following TBI including explicit and spatial memory. While the effects of linear impacts forces have been widely characterized, studies of the effect of angular acceleration induced TBI are still very limited. To further investigate this, we developed a novel model of rotational TBI to study the effects on parameters of neuropathology. Currently, no therapeutic exists to treat TBI, and an accurate, clinically relevant understanding of brain injury is the first step towards therapeutic intervention. Previously, our lab has reported TBI induces aberrant activation of cyclin dependent kinase 5 (cdk5) as a principal perpetrator of neuronal death following brain injury and genetic knockdown of cdk5 is neuroprotective. We observe aberrant cdk5 activity within our novel rotational model of TBI and hypothesize cdk5 may mediate neuropathological outcomes following injury. Here, we characterize a novel brain permeable cdk5 inhibitor as a potential post-injury therapeutic. We examine the effect of post-injury administration by assessment of hippocampal histopathology, electrophysiology, and behavior. This research is the first step in understanding how rotational TBIs are mediated by aberrant signal transduction, the mechanisms involved, and how treatments targeting this aberrant signaling may be used to improve outcomes for brain injury TBI patients.




Additional Abstract Information

Presenter: Raegan Adams

Institution: University of Alabama at Birmingham

Type: Poster

Subject: Biochemistry

Status: Approved


Time and Location

Session: Poster 1
Date/Time: Mon 1:30pm-2:30pm
Session Number: 2119