In the materials noted here, a Buck Institute researcher puts forward a view of just one side of the science of advanced glycation end-products (AGEs) and their role in degenerative aging. AGEs are sugary metabolic byproducts of many different varieties, both present in the diet and generated in the body. In the view of AGEs and aging expounded here, near all of the many types of AGE are important, most are transient and levels will vary in response to day to day circumstances, dietary intake of AGEs probably has a significant negative influence on long-term health, and AGEs present in tissues disrupt metabolism by hammering on a set of receptors that trigger chronic inflammatory signaling and a range of other inappropriate cellular behavior.
This leads to proposals for interventions that run along the lines of eating a better diet, finding ways to block the interaction between AGEs and receptors such as RAGE and RANKL, and so forth. If successful, these approaches could be expected to slightly slow the pace of aging, largely via reduced levels of chronic inflammation. It isn’t an unreasonable viewpoint: the evidence for AGEs to cause inflammation is fairly robust; the involvement
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