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Saturday, June 25, 2005

gene expression and the search for the fountain of youth

Interesting article on the use of microarray technology at several research labs to elucidate the mechanism of aging, from nematodes to humans.

Kenyon is determined to find out how much a 959-cell worm can really tell us about cell death, and, by extension, aging in humans. "People said to me, 'Why study the worm? You won't learn anything about people from studying the worm.' They were all totally wrong. Turns out there is a whole set of genes whose only job in the world is to determine the pattern of an animal. The reason a dog looks different than a cat is that some of those genes are turned up or down, but they're the same genes."

Another common misconception, says Kenyon, is that people just get old, and nothing can be done about it. "I thought that there must be some kind of machinery, like a clock, that controls the rate at which the animal ages," she says. "The clock can be set to go fast in a mouse, which has a two-year life span, or it can be set to go slowly in a human, which has an 80-year life span. We began to change genes at random to see which ones influence life span, and we found [the] daf-2 [gene]."

By adding copies of daf-2 to C. elegans, Kenyon and others were able to expand the worm's life span sixfold. "Everybody who sees our long-lived worms thinks they're magic," she says. "What we find in these model organisms is [when we] change gene activitives, we don't just increase life span, we also postpone the time of onset of a lot of different age-related diseases. The goal is to do both. There are worms that are long-lived and don't appear to be healthy. That, to me, is the nightmare."
See the full article from Genomics & Proteomics magazine.

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