June 19th, 2026
Adjusting the operation of metabolism to modestly slow aging has long formed the bulk of fundamental research into intervention in aging. All living organisms exhibit some plasticity of life span when subject to mild stresses, such as lack of nutrients, heat, cold, and so forth. Unfortunately this strategy seems unlikely to lead to therapies that greatly improve upon the effects of exercise and lifestyle choice, particularly given the evidence for metabolic adjustment to produce ever smaller gains in longevity as species life span increases. Nonetheless, this form of research persists, driven by the scientific urge to obtain complete understanding of the way in which aging progresses in detail. Here, for example, researchers provide evidence for there to be multiple options for the adjustment of metabolism to slow aging, not just one path.
While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. Our previous work has shown that targeting aging pathways can be neuroprotective in animal models of neurodegenerative disease. Based on these findings, we believe that by gaining insight into the aging process, that knowledge can be applied to identify novel therapeutic targets for neurodegenerative disease. To advance our understanding of aging, we used a genomics approach to identify genes regulated by multiple lifespan-extending pathways. We performed RNA sequencing on nine long-lived C. elegans mutants representing seven longevity pathways: insulin/IGF-1 signaling, dietary restriction, germline deficiency, impaired chemosensation, reduced translation, elevated mitochondrial reactive oxygen species (ROS), and mild mitochondrial impairment.
