ER Stress and Oxidative Stress Mechanistic Studies

Endoplasmic reticulum (ER) stress is a cellular stress response that is activated in order to cope with cellular homeostatic challenges. In early or mild activations, ER stress is protective. However, with prolonged or severe challenges, ER stress can cause apoptotic cell death. Additionally, there is a significant role for oxidative stress, and these two stress pathways highly overlap. Thus, we are interested in understanding their relationship after TBI and whether interfering with certain aspects of this relationship might prove more beneficial than targeting only one process.

Understanding the Role of Systemic Inflammation in TON/TBI Outcomes

TON triggers inflammation at the injury site, leading to degeneration and death of nerve cells in the eye and optic nerve. Head trauma also leads to systemic (i.e., in the whole body) inflammation, which we have found likely plays a role in secondary injury to the optic nerves. Ongoing research in the lab seeks to find ways to alter this inflammation to improve outcomes after optic nerve trauma.

Determining the Influence of Chronic Stress on TBI Outcomes

Adolescence represents a critical period of increased vulnerability to stress, which increases in chronic illnesses such as TBI. We are interested in the effect of chronic stress on brain pathology after head trauma. Because axonal degeneration after TBI is associated with glial cell activation, we also focus on how microglial and astrocyte functions are chronically altered after TBI.

Our lab is interested in the effects of secondary injury on TBI pathophysiology and biology. By leveraging the optic nerve as a model of TBI-induced axonal injury, we hope to better understand the mechanisms that govern secondary injury cascades. By determining which pathways are important, and how they interact we can provide better insight into how long-term outcomes develop and potential ways to prevent them.