What inspired you to pursue aging research?
When I started studying osteoporosis, it was largely focused on genetics and in adult animals, but I was always curious about all the changes that occur during aging. This led me to seek training in the biology of aging and pursue projects that were more specific to age-related mechanisms of bone loss. What really excited me was the Geroscience Hypothesis, where targeting aging mechanisms (such as cellular senescence) is proposed to alleviate tissue dysfunction across a broad range of organs. This is such an attractive idea and has drawn me to pursue aging research as a major focus of my scientific career.
In your view, what does AFAR mean to the field, and what does it mean, for you, to receive an AFAR grant now?
Having an incredible organization such as AFAR allows scientists at all stages of their careers to pursue projects that may otherwise be unfunded by other entities. AFAR’s focus on the biology of aging has led to so many incredible discoveries that have unraveled the complexities of aging and pushed the field forward in an unprecedented way. Particularly in this tumultuous funding climate, funding from AFAR ensures that the wheels of progress will continue to turn in the aging field. As I start my own laboratory, this AFAR grant will be incredibly valuable in the development of my research program and will support our ongoing work at a time where funding from other sources is in jeopardy. This funding allows us to pursue a project that will open many avenues for future projects, and I cannot be more grateful.
What is exciting about your research’s potential impact?
If our hypothesis is correct, then post-injury senescence may be established as a new driver of accelerated aging. This is exciting because we are always looking for new causes of aging, and as senescence can be targeted by senolytic drugs, this aspect could be treatable. As injuries and acute insults occur to organs all across the body, the success of this work would justify the study of post-injury senescence in other tissues as drivers of age-related dysfunction and disease.
How would you describe your research to a non-scientist?
With age, cells in the skeleton accumulate damage and become “aged”, resulting in bone loss and an increase in fracture risk. Besides aging, these damaged cells also appear after bone fractures, even in youth, and linger beyond the completion of fracture healing. This suggests that injured bones may resemble a prematurely aged tissue and predispose individuals to higher rates of bone deterioration and fracture in old age. Our work will study this phenomenon to understand how to identify and therapeutically target these residual, post-fracture damaged cells to improve skeletal health. The success of this project will establish injury as a driver of accelerated aging, which may extend to other organs.
