IBSC-BME PhD Defense Announcement for Edmond A. Rogers (R. Shi, advisor)

Everyone is invited to attend the public presentation beginning at 10:30 AM.

Title of Thesis Research: Elucidating pathological correlations between Traumatic Brain Injury and Alzheimer’s Disease

Committee:

Major Professor: Dr. Riyi Shi, M.D., Ph.D.

Dr. Fang Huang, Ph.D.

Dr. Joesph Rispoli, Ph.D.

Dr. GuangJun Zhang, M.D., Ph.D.

Date/Time: April 5^th at 10:30 AM – 12:30 PM

Location: https://purdue-edu.zoom.us/j/97333625618

Abstract:

Traumatic Brain Injuries (TBI) are a major cause of disability and death in the United States. One of the greatest consequences of the disease is the resulting long-term damage, especially in milder injuries where the damage is initially subclinical and thus lacking acutely observable manifestations that over time can compound significantly. Among these chronic issues, Alzheimer’s Disease (AD) could be the most serious. While multiple studies demonstrate an increased likelihood of developing neurodegenerative diseases in response to TBI, the underlying mechanisms remain undefined and limited treatment options are currently available. Multiple hypotheses have been postulated based on various animal and clinical models, contributing a great deal to our current knowledge base and implicating several related-targets of interest (i.g. oxidative stress, inflammation, proteostasis-disruptions). While extremely valuable, these in vivo examinations are physiologically and ethically complex: there is currently no model capable of separating and visualizing TBI-induced sub-cellular damage in the moments immediately following injury, and the associated long-term changes. Further, no mechanistic study has been performed to link mechanical-trauma independently with neurodegeneration initiation via protein aggregation. It is clear that additional investigative tools are needed to rectify these intricate issues, and while in vitro methodologies generally offer the type of resolution required, no such model replicates these phenomena. Therefore, we introduce the “TBI-on-a-chip” in vitro concussive model, with a series of concomitant targeted-experiments to address this urgent, currently unmet need. Utilizing TBI-on-a-chip, we directly observe evidence of impact-induced functional and biochemical consequences, while isolating oxidative stress as a key, contributing component.