Research Interests:
Nicotinamide adenine dinucleotide (NAD+) levels have been shown to decline with age and remain depleted during disease states. Increased levels of NAD+ consuming enzymes (e.g., Sirtuins, PARPs, CD38) contribute to the decline of NAD+ with age, resulting in mitochondrial dysfunction and inflammation. Disease and age-related functional decline can be mitigated by boosting NAD+, which can be achieved by administering its precursor, NMN. As an undergraduate at Simmons University, I conducted my thesis on the use and characterization of a novel zebrafish model to understand the genetic and metabolic regulation of aging and the application of preventative aging mechanisms. I’m now interested in developing a library of small-molecule NAD+ precursors to combat the adverse conditions of aging and mimic the effects of exercise, particularly in aged skeletal muscle.