What inspired you to pursue aging research?
Aging is a new direction for me. My research has been focused on understanding the genome, especially the 98% of the DNA sequences in the genome that have long been thought to be noncoding, i.e., do not code for proteins. New genomic technologies have revealed that many of those noncoding sequences are actually copied into RNA and translated into proteins, and such noncanonical translation activities are increased during aging and neurodegeneration. Our preliminary studies also suggested that these noncanonical translation activities may interact with other cellular processes and together they drive aging progression. We are very interested in understanding more about aging from the perspective of how genetic information is coded in the genome and then decoded by cells.
In your view, what does AFAR mean to the field, and what does it mean, for you, to receive an AFAR grant now?
By supporting bold ideas, especially from junior faculty with no prior experience in aging research, AFAR and the Glenn Foundation encourage innovative research that will ultimately benefit the aging field. The support for our project allows us to test an out-of-box idea that has the potential to become the main focus of my lab. It also allows me to train a new generation of scientists who will continue to study aging biology with genomic approaches.
What is exciting about your research’s potential impact?
If successful, our research will establish a new paradigm for aging progression, i.e., via self-reinforcing feedback loops. It will open new lines of research into the complex interplay between multiple hallmarks of aging. It will also lay the foundation for developing new healthspan-extending interventions that target the feedback loop.
How would you describe your research to a non-scientist?
Natural aging is a unidirectional decline of normal functions of organs and cells. In both engineering and biological systems, unidirectional processes are often driven by positive feedback loops that can reinforce an initial perturbation and push a system towards extreme states. We will test the idea that natural aging is driven by such a self-reinforcing feedback loop, and specifically a feedback loop that amplifies errors in the fundamental processes of how genes in the genome are decoded by cells. This is largely due to the fact that 98% of our genome is not coding for genes. We will test our idea in mice. Our study has the potential to uncover new interventions that could delay aging in humans.
