Abstract
The “network” of homeostatic systems fails in distinct ways in individual isogenic animals during the aging process. We believe that understanding these distinct physiological states, the transitions between them, and how they relate to homeostatic system functions will allow us to better affect change in the aging process. Work in yeast showed that fixing an initial system failure, loss of vacuole acidification capacity, could increase cellular lifespan. Here we showed how the long-lived physiological state conferred by high expression of the hsp-16.2 promoter based lifespan/penetrance biomarker correlates with differences in the expression of other genes, and the structure and function of lysosomes. We found that vacuole acidification failure is not a major initial proximal cause of aging in C. elegans – at least not in their intestine cells.
Highlights
Traditional approaches aimed at delaying or preventing age-dependent diseases view each disease as a distinct entity, resulting from separate pathophysiological chains of events
University of Arizona, Tucson, Arizona, United States. This session will focus on interventions to delay biological aging with the goal of in increasing lifespan and healthspan
By manipulating kynurenine pathway enzymes and metabolites, we have extended lifespan up to 40% in Caenorhabditis elegans
Summary
Traditional approaches aimed at delaying or preventing age-dependent diseases view each disease as a distinct entity, resulting from separate pathophysiological chains of events. Lifespan by slowing age-associated accumulation of oxidative damage and repressing chronic inflammation. The second domain will be activities of daily living where the subjective measure is perceived effort and the objective measures include various data from sensor such as EDA (arousal) and EMG (muscle contraction). INTERVENING IN THE LONGEVITY NETWORK Chair: Alexander Mendenhall, University of Washington, Seattle, Washington, United States Co-Chair: George L.
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