TEDGlobal 2011- Cynthia Kenyon: Experiments that Hint at Longer Lives

Video Link: http://www.ted.com/talks/cynthia_kenyon_experiments_that_hint_of_longer_lives.html

Speaker's Bio (from TED):

Cynthia Kenyon is revolutionizing our understanding of aging. As an expert in biochemistry and biophysics at the University of California at San Francisco, she is particularly interested in the influence that genetics have on age-related diseases (from cancer to heart failure) in living things.

Her biggest breakthrough was figuring out that there’s a “universal hormonal control for aging”: carbohydrate intake, which can have a dramatic effect on how two critical genes behave, reducing insulin production and boosting repair and renovation activities. So far, her theory has proved true for worms, mice, rats, and monkeys — and she suspects it applies to humans, too.

By studying aging, Kenyon believes that she and other scientists (many of whom have successfully duplicated her experiments) will be able to pinpoint the molecules responsible for the onset of age-related diseases in people and prevent them. She’s co-founded a drug-development company called Elixir Pharmaceuticals to do just that.

She says: "The link between aging and age-related disease suggests an entirely new way to combat many diseases all at once; namely, by going after their greatest risk factor: aging itself."

"Ten years ago, we thought aging was probably the result of a slow decay, a sort of rusting. But Professor Kenyon has shown that it’s ... controlled by genes. That opens the possibility of slowing it down with drugs."

Jeff Holly, Bristol University

Summary:

Different animals have different lifespans (i.e. mice- 2years, v. bat- 50 years) There must be something in the genes for aging, so you should be able to change the aging gene to expand life span.

They did experiments on a roundworm and found that mutations that damage a gene called daf-2 could double the worm’s lifespan. The daf-2 gene encodes a hormone receptor which promotes aging. (similar to the ones that promote food uptake and growth.)

They did the same mutation in flies and mice, and it worked on them.

People who lived to 90-100 in a population of Ashkenazi Jews were more likely to have mutations to daf-2 which would make it work less well. They are also less susceptible to things like cancer and age related deseases.

She explains how and why it works.

Follow-up questions about- Certain animals that don’t have aging. And can we do this by changing genes instead of developing a medication. (She says that would be a bad idea).