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Mutations in this gene cause worms to live 50% longer than usual. A few months later, two more clock genes were discovered, and worms with combinations of mutations on these genes had a much more dramatic increase in longevity. Some of these combined mutations caused worms to live four times longer than normal. When daf-2 mutations were associated with the clock mutations, worms lived up to seven times longer than normals.
"Pharmaceutical interventions that slow aging might delay the onset of neurodegenerative diseases."
How do clock genes work? Probably by influencing metabolic rates. Long-living worms with mutated clock genes have a lower rate of metabolism than their normal counterparts. How could metabolic rates affect aging? The link is probably free radicals. High metabolic rates cause more free radicals to be formed. These results suggest the tantalizing possibility of increasing life-span either by slowing the production of free radicals, or by increasing free radical scavenging.
Yet another gene points towards oxidative damage as a primary cause of aging. This time the gene was discovered in fruit flies and was named methuselah, in honor of the Biblical Methuselah who reportedly lived to be 969 years old. Fruit flies with a mutated methuselah gene live 100 days, instead of the usual 60 to 80 days. How does the mutant methuselah gene work? Like the long-lived worms, the long-lived flies were able to better resist a number of stresses. They survived 50% longer than their wild-type counterparts when deprived of food. They tolerated heat much better. They were more resistant to paraquat, a herbicide that resembles MPTP, and kills cells by generating free radicals. Recently, increased resistance to stress has also been shown to lengthen life in yeast.