Chronological age is the primary risk factor for deadly late-life illnesses such as cancer, heart disease, and neurodegeneration – diseases to which most of us will eventually succumb. However, we spend the vast majority of our research resources on a disease-by-disease basis, rather than addressing their root cause: aging.
Even a hypothetical cure for a given aging-related disease would increase lifespan by only a few years. Likewise, lifestyle modifications such as regular exercise only boost lifespan by one or two years at most. In contrast, interventions in the aging process itself can increase lifespan by much greater factors.
In mice, changes in single genes can extend longevity by 25-50%; in smaller and more genetically tractable organisms such as worms and flies, multiple simultaneous interventions have increased lifespan by as much as fourfold. From genetic studies, we know that aging in humans is governed by many of the same mechanisms as in the model organisms we use in the lab. It therefore seems reasonable to claim that intervening in the aging process holds the promise for a much greater return on resource investment than the disease-by-disease approach currently favored by the status quo.
Patil’s main goals for this presentation will be twofold:
Throughout the presentation, Patil will emphasize the potential connections between basic and translational research – that is, between the lab bench and the hospital clinic – over both the near and long terms. Another important theme will be the requirement for collaboration across interdisciplinary lines, the essential contribution of the “open science” approach to the success of such collaborative efforts, and the importance of developing tools that empower collaboration and openness.
I am a biogerontologist (a molecular and cellular biologist of aging) currently working to understand the changes in gene expression that occur during cellular senescence, a fundamental aspect of the aging process in mammals.
My past training is in studies of cellular stress; as a graduate student, I was an early adopter of microarray expression profiling technology. My thesis project combined microarray technology with classical genetic analysis and computational modeling to allow a study of cellular stress responses at the whole-genome scale.
I try to bring an open, collaborative and interdisciplinary perspective to my experimental work. I’m particularly excited about a new multi-institute collaborative project that will test dozens of hypotheses about the mechanisms of aging in dozens of different species, in parallel.
When I’m not working at the bench, I write about recent developments in biogerontology at my weblog, Ouroboros: Research in the biology of aging .