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Wednesday, December 6th 2006

The Price Of Aging

The longer you live, the more mutations you develop. Which is why so many cancers have a prevalence later in life. One of your body’s methods for fighting this fact is to decrease cell division. But that decrease in the production of new daughter cells may be a key process in aging. Is that the trade off we’re making?

Of the 10 or 15 molecules dedicated to cell division, only one accumulates with age: p16INK4a (p16 for short), which can be 100 times more abundant in the tissues of older people than in young people. Researchers know that the protein stops cells from dividing; without it, most large moles would probably become skin cancer. What they didn’t know was whether the protein also hinders healing and regeneration as we grow older.

[T]o study regeneration…[they] selectively destroyed the mice’s pancreatic cells using a particularly toxic chemotherapy drug.

Within 100 days, he saw two distinctly different outcomes. If an old mouse was p16-deficient, it regrew pancreatic cells and cured itself like a normal young mouse. If it had a normal p16 gene that curbed cell division, it died of diabetes.

“Basically you’ve got a choice,” says Morrison. “You can either die of aging or die of cancer. But you’re gonna die either way.”

Interesting. Here’s the abstract of the study in Nature, and the full article if you have a subscription.

H/T Reddit

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