While model organisms like fruit flies have been invaluable in identifying hundreds of genes associated with aging, there is still concern that any increases in fly lifespan simply cannot be expected to work in mammals. Kennedy and his group examined this issue by carefully analyzing age-related genes in yeast and the C. elegans worm, two organisms that diverged over a billion years ago.

They found a statistically significant connection in the genes and pathways that affect aging in both organisms, including reduced mTOR signaling. They suggest that the conservation of aging genes across animals exists not because specific genes have evolved to regulate aging, but rather because animals have evolved a similar response to nutrient restriction, and lifespan is tightly linked to this response, providing evidence that efforts in humans just might work.

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