Assistant Professor, University of Southern California
Glenn Foundation for Medical Research and AFAR Grants for Junior Faculty - 2022
What inspired you to pursue aging research?
As someone who worked in the hustle and bustle restaurant environment of New York City, high stress was an everyday phenomenon. We always hear the dogma of “stress is bad for aging”, and thus as someone who was constantly in high stress environments, I was very curious about what actually happened on the cell biological level when one was constantly inundated with stress, and ultimately how this impacted aging. Through my research experience, I was able to slowly begin to understand how stress impacts aging by understanding the concept of stress resilience – our capacity to respond to stress. Now, the Sanabria Lab investigates how stress resilience declines during aging, and what we can do to maintain high stress resilience as a means to combat age-related decline in health.
In your view, what does AFAR mean to the field, and what does it mean for you to receive an AFAR grant now?
AFAR plays a truly remarkable role in redefining the field of aging by supporting scientists—primarily young scientists—in the cutting-edge research, focusing primarily on the impact of the researcher and project to the field, rather than focusing solely on currently existing preliminary data that many other funding agencies may prioritize. This allows for breakthrough discoveries from truly innovative ideas to redefine science in novel ways. As a new scientist, the AFAR is an incredible opportunity to allow my lab to create a new niche in aging biology—a feat that would be impossible without the support.
What is exciting about your research’s potential impact?
Perhaps most exciting about my research’s impact is that it ascribes a critical function of neurons to coordinate an organism-wide response to stress. This may allow future studies to combat aging by focusing solely on neuronal health. Since neurons can drive stress resilience within the entire organism, could it be possible that anti-aging therapies that focus on stress resilience be targeted solely to neurons with the potential that neurons can coordinate the entire body to respond similarly, despite not being exposed to a therapeutic agent? This would be astounding as much smaller amounts of therapeutic agents would be necessary with a neuron-focused intervention.
How would you describe your research to a non-scientist?
The Sanabria lab studies the intersection between stress and aging, trying to understand how stress impacts the aging process and how aging alters an organism’s capacity to deal with stress. We use diverse genetic tools to identify mechanisms that impact stress resilience: that is, an organism’s capacity to return to normal health after exposure to stress. Most specifically in this project, we study how neurons can actually serve as a “gatekeeper” of stress: that is, neurons can sense stress and signal to the rest of the body to response to stress. This research is particularly exciting because it may show that preserving neuronal stress responses may be sufficient to combat aging (rather than having to target the entire body), as neurons can signal to all other cells and thus recruit other parts of the body to elicit a similar response.
