Aging is one of the greatest mysteries in biology, and arguably its next frontier. Old age is the main risk factor for many disorders, including cardiovascular disease, cancer, diabetes, and Alzheimer’s disease. Yet our understanding of aging is still rudimentary because aging is an extraordinarily complex process that defies many conventional rules of biology.
Key unanswered questions that fascinate us are: What are the causes of frailty and sarcopenia? Can these features be reversed?
To address these questions while reflecting on the complexity of aging, we developed a vibrant research program based on a translational approach, clinic to bench and back to the clinic. Our research lab is deconstructing frailty and sarcopenia into its most fundamental questions using preclinical animal models (mice and rats). We’ve already broken new ground by pioneering physical therapy clinical assessments with our preclinical animal models.
Examples of exciting phenomena we have discovered include:
- Skeletal muscle and muscle fiber type specific age-related loss in contractility (strength, power)
- Age-associated post-translational modification of key muscle proteins and critical amino acids
- Protein expression and metabolic alterations with aging
- Alterations in protein degradation with aging, and the development of a frailty index/phenotype in mice
In the future, we plan to use the mouse frailty phenotype to delve into the mechanisms contributing to muscle dysfunction, independent of age.This research has the promise to transform our understanding of aging, frailty, and muscle which are at the heart of many human diseases and poor quality of life.