Dong Lab

OxPCs are byproducts of oxidative stress which are increased in acute and chronic MS brain lesions. Yet, how OxPCs contribute to chronic damage in the brain and spinal cord during progressive MS remain mostly unknown. We aim to determine how OxPCs propagate inflammation and chronic injury in the aging brain and spinal cord white matter and grey matter, and to identify new therapeutic strategies to help treat progressive MS.

Phosphatidylcholines (PCs) are major constituents of the cell membrane that separates DNA and other cellular structures from the outside environment. Like all other molecules involved in normal biological processes, PCs are constantly degraded and recycled. However, when oxidative stress occurs, such as during inflammation, PCs can be converted into OxPCs. Abnormal accumulation of OxPCs can cause cell death and propagate excessive inflammation. Thus, organisms need a way to eliminate OxPCs, but these mechanisms are not well understood. In this project, we aim to understand the how tissue resident macrophages use cell surface scavenger receptors such as TREM2 to neutralize OxPCs during inflammation.

Exercise is emerging as an intervention for promoting regeneration and remyelination in MS. Since exercise also has potential anti-aging and antioxidative effects, our objective is to test the ability of long-term exercise to neutralize oxidative stress and to help reduce pathology in chronic MS lesions. By identifying the neuroprotective mechanisms induced by long-term exercise, it may be feasible to therapeutically activate the protective benefits conferred by exercise to help people with limited mobility.