Olivia Kane
Research Mentor(s): Joseph Wider
Mentor Department:
Authors: Olivia Kane1, Reagan Speas1,2,3, Sarita Raghunayakula3, and Joseph Wider PhD3
Session: Session 2 (10:00am – 10:50am)
Presentation Type: Poster 2
Abstract
Traumatic brain injury (TBI) is a neurological condition caused by a forceful jolt or blow to the head. TBI is the leading cause of disability worldwide, impacting millions of individuals each year and leading to a vast array of chronic physical, cognitive, and behavioral impairments. Previous research suggests that mitochondria are ideal targets for TBI research in both pathophysiological phases: primary, which occurs immediately after the injury with varying severities (e.g., mild, moderate, and severe), and secondary, which lasts from minutes to years. Mitochondria play a role in neuronal energetic regulation, which is regulated through dynamics, coordinated cycles of fission, mediated by Drp1, and fusion, mediated by Opa1. We hypothesize that mitochondrial dynamics are disrupted during progression of secondary TBI in a severity-dependent manner. Primary cortical mouse neurons were grown in BioFlex® 6 and 24-well plates and impacted at 20, 35, and 50 psi using a Cell Injury Controller II (21-087) to simulate mild, moderate, and severe TBI. Samples were collected at control, 0, 1, 2, 3, and 4 hour timepoints for Western Blot to quantify Drp1, Opa1, and Oma1 expression and mitochondrial morphology data. This study found [RESULTS TBD]. Thus, by exploring the impact of TBI severity on mitochondrial morphology and dynamics, this research sheds light on potential interventions that will improve outcomes for TBI patients.
