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Characterization of Neuropathology and Neuroinflammatory Cascades After Mild TBI in Swine

Wednesday, December 9, 2020

1:00 PM-3:00 PM

BIOMED PhD Research Proposal
Characterization of Neuropathology and Neuroinflammatory Cascades After Mild Traumatic Brain Injury (TBI) in Swine

Michael Grovola, PhD Candidate
School of Biomedical Engineering, Science and Health Systems
Drexel University

Catherine von Reyn, PhD
Assistant Professor
School of Biomedical Engineering, Science and Health Systems
Drexel University

D. Kacy Cullen, PhD
Associate Professor of Neurosurgery
Department of Neurosurgery
Perelman School of Medicine
University of Pennsylvania

Traumatic Brain Injury (TBI) is caused by a mechanical insult to the head and often results in prolonged or permanent brain dysfunction. TBI represents a major health and socioeconomic problem; in the U.S. over 2.8 million are affected annually. Even so-called “mild” TBI – otherwise known as concussion – may induce neurophysiological deficits affecting learning, memory, and concentration that do not resolve in up to 15-20% of patients. There are currently no approved treatments to improve recovery from TBI. Our previous studies in this model have shown that mild TBI is not associated with frank neuronal loss, but rather subtle changes in synaptic loss or gain and neuronal hypertrophy occurring concomitantly with migration and activation of microglia – the resident immune cell of the central nervous system.

Though the precise role of microglia following TBI is still unclear, they have been shown to phagocytose cells and modify synapses under normal and other pathophysiological conditions. To elucidate the role of microglia and the neuroinflammatory response to mild TBI, we will conduct in-depth histological profiling of neuroinflammation after mild TBI in discrete neuroanatomical regions across three specific aims using a porcine model of TBI. Our model is the most clinically relevant model of closed-head diffuse TBI in use today, as it closely replicates human head injury biomechanics that cannot be reproduced in small animals.

In Aim 1, we will assess the relationship between hallmark white matter pathology and potential microglia activation at chronic time points after diffuse TBI. In Aim 2, we will examine neuroinflammatory and synaptic changes in the hippocampus, a region known to be susceptible to damage following TBI. Finally, Aim 3 will expand on our lab’s discovery of a novel mechanism of immediate membrane disruption in cortical somata that initiates neuroinflammation after TBI. This gray matter pathology may be highly relevant as closed-head diffuse TBI has generally been considered to feature white matter pathology. The proposed studies will increase our understanding of the neuropathological consequences of mild TBI. Overall, the current proposal is a critical step in identifying inflammation-related degenerative pathology that may underlie the cognitive, behavioral, and motor dysfunction that millions of Americans experience as a result of TBI.

Contact Information

Natalia Broz

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