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| NIH Profile: Cynthia Kenyon, Ph.D. |
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Like Death and Taxes? Cynthia Kenyon debunks the notion that aging is inevitable. The average roundworm, called C. elegans, lives about 21 days. Manipulate a single gene, and its lifespan jumps to 45 days. Toy with its reproductive cells as well, and it will live four times longer than normal. Similar age-enhancing effects can be seen when the same genes are changed in fruit flies and mice. But what can these odd animals tell us about the way humans age? "Lots," says biochemist Cynthia Kenyon, Ph.D. Animals might look very different, but at a basic level, things are very similar. "All animals are made of cells. Muscle and nerve and intestinal cells are incredibly similar between people and any of the animals we use as model organisms in science." The muscle fibers of the tiny worm look the same as ours. The genes that plan how the body develops are similar as well. "It's a little bit humbling to realize how similar we are to primitive, simple animals," admits Kenyon, a 50-year-old professor of biochemistry at the University of California at San Francisco. "But that's the way it is." It makes Kenyon's research enthralling. With support from the National Institute on Aging, her team discovered 10 years ago that a single change in the DAF2 (decay accelerating factor) gene, which encodes a receptor similar to the human receptors for the hormones insulin and IGF-1, doubled the worms' lifespan. Because the same pathways have been shown to affect lifespan in fruit flies and mice, it's possible that they affect lifespan in humans as well. The striking thing is that the gene mutation doesn't just delay aging, it postpones the diseases of aging as well. In 2002, Richard Morimoto's team at Northwestern University changed the DAF2 gene in a strain of C. elegans that develops Huntington's disease. The worms got Huntington's, but later. Same for mice: they get cancer, but not until they're older. Kenyon's lab went on to show that this occurred because DAF2 controls other genes that prevent abnormal proteins, like the Huntington's protein, from clumping together — the hallmark of this disease. In June 2003, the researchers reported results using DNA microarray technology to trace all the genetic changes that flow from that single DAF2 change. They found that DAF2 exerts its influence through genes that fight infection and control metabolism, through genes that control the cell's response to stress, and by dampening the activity of specific genes that shorten life. In short, DAF2 turns up expression of many different genes, each of which helps out in its own way. "The consequences are stunning," Kenyon says, "and if we can figure out a way to copy these effects in humans, we might all be able to live very healthy long lives." She says looking at these longer-living worms is exactly like looking at a 90-year-old who is indistinguishable from a 45- year-old in every way. That motivated her to launch a company called Elixir to develop and find drugs that can have the same impact and get them to market. "It's a wonderful thing that society has done — created a fabulous basic research operation and then a complementary biotech industry that moves the basic research to the clinic," she marvels. "I'm not saying there will be a pill to double lifespan immediately," she warns. "But if it worked in worms and now other animals, we're faced with possibilities we never saw before." The drugs that eventually succeed, she predicts, will be those that affect the diseases of aging. "Many people might question whether we want to expand lifespan, but there's no question about staying healthy and avoiding diseases."
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This page was last reviewed on April 26, 2005 . |
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National Institutes of Health (NIH) |
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