(252g) Human aging and senescence at single-cell resolution

Most older adults are affected by multiple chronic diseases and have an increased risk of developing physical and cognitive disabilities. However, the inherent variability observed among older individuals indicate that this risk of disability and disease is not uniform. As such, there is a critical need to develop new approaches to capture the underlying biological mechanisms of aging that describe disease susceptibility and resilience in older adults. A growing body of evidence shows that the interactions of intrinsic and extrinsic factors, across length scales from molecules to organisms, contribute to the rates of ageing and age-associated diseases in humans. However, it is unclear how underlying molecular states of an individual relate to their clinical outlook. We postulate that studying age-related changes at intermediate length scales of cells may provide a key link to understanding ageing patterns in humans. As integrators of molecular signals, cells offer a sensitive mesoscale view of ageing, with cellular dysfunctions likely occurring prior to the manifestation of age-related diseases. My lab is interested in developing new technologies and approaches to map aging trajectories based on the properties of cells. Our hypothesis is that if we can map healthy aging, then deviations from healthy aging trajectories can inform on disease states.
In my presentation, I will focus on how biophysical properties of cells constitute a framework to study aging and senescence in humans, the role of cellular heterogeneity in propagating aging and aging-related phenotypes, and a generalizable framework to understand emergent patterns of single-cell motility with applications beyond aging in health and disease. Through this work, we are seeking to develop a better understanding of why humans age differently, with the goal of developing precision aging strategies to eventually impact the health of aging individuals.