Our research program can be summarized by the adage, “Food is medicine.” We believe that food and nutrition reside at the center of healthy aging and seek to determine how certain food-derived compounds and dietary practices preserve health, whereas others promote disease.

Our lab projects focus on how cells adapt to stresses and how nutrition impacts these responses. A central theme guiding our work is that healthy aging requires cells to retain the capacity to sense stressors like oxidative stress, starvation, and hyperglycemia, and then respond to restore homeostasis. Failure to neutralize stresses in a timely manner results in inflammation, tissue damage, and loss of organ functions. We are particularly interested in understanding how the transcription factor Nrf2 functions to maintain resiliency and prevent disease in the context of neurodegeneration and autoimmune disorders.

A main project in the laboratory involves determining how very low-carbohydratediets impact the motor and visual deficits observed in multiple sclerosis. These studies utilize a mouse model of MS with the goal of developing nutritional intervention strategies that people with MS can leverage. At the mechanistic level, we are exploring how restricting dietary carbohydrates accelerates resealing the blood-brain barrier and how various populations of immune cells can be converted from pro-inflammatory to anti-inflammatory as a function of diet.

A second project investigates the therapeutic potential of sulforaphane, a potent activator of the Nrf2 transcription factor, that is derived from cruciferous vegetables including broccoli, Brussels sprouts, and kale. To date, our studies have shown that this compound can mimic a fasting response and preserve vision in a mouse model designed to mimic features of age-related macular degeneration (AMD), a leading cause of irreversible vision loss in people over the age of 65.

My Publications