David Sinclair· PhD
Back in 1993, Kenyon discovered a single-gene mutation that could significantly impact the lifespan of C. elegans. Moreover, she showed us that the mutation could be reversed.
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The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
Back in 1993, Kenyon discovered a single-gene mutation that could significantly impact the lifespan of C. elegans. Moreover, she showed us that the mutation could be reversed.
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Kenyon's discovery helped push a new generation of aging researchers (including me) to intensify the search for an evolutionary-conserved program that influences aging in all organisms — a potential single cause.
So Cynthia in worms and then Lenny in yeast, where I was at MIT, made the finding that a single gene alteration can have a huge impact on an organism's lifespan.
And when she cloned the gene and found out where it was, it was in a gene that sensed insulin, it's the insulin receptor gene called DAF-2.
But we're going to start in the 1990s with Cynthia Kenyon and her work on sea aliens.
And she mutated them and found a strain of worm, a mutant worm, that was living twice as long; so instead of living for 15 days, 30 days.
i remember reading a review piece from cynthia where she said the genetic mutations in worms that cause doubling of lifespan show that organisms have the capacity to live longer than they normally do