Gene Found to Switch Off Stem Cells During Aging - New York TimesNote the implication that you can now measure someone's biological age by their Ink-4 protein production. I've long thought that aging was non-linear, that we age in bursts (much as the folk story of 'he aged a year in a day'), possibly triggered by environmental events. It would be interesting to plot weekly Inf-4 levels in 20 individuals over the course of 2 years.
September 6, 2006
By NICHOLAS WADE
Biologists have uncovered a deep link between lifespan and cancer in the form of a gene that switches off stem cells as a person ages.
... The gene involved in the new finding has the unmemorable name of p16-Ink4a but plays a central role in the body’s defenses against cancer. It produces two quite different proteins that interact with the two principal systems for deciding whether a cell will be allowed to divide.
One of these proteins had also been noted to increase substantially with age. The cells of a 70-year-old person produce 10 times as much of the Ink-4 protein as do those of a 20 year-old, Dr. Sharpless said. To help understand why this was so, Dr. Sharpless genetically engineered a strain of mouse in which the gene was knocked out.
... All three teams report essentially the same result, that in each type of tissue the cells have extra ability to proliferate when the Ink-4 protein can no longer be made. At the same time the Ink-less mice are highly prone to cancer, which they start to develop as early as one year of age.
... a calorically restricted diet is one intervention that is known to increase lifespan and reduce cancer, at least in laboratory mice. The reason, he said, is probably because these diets reduce cell division, the prime source of cancer risk...
... Dr. Morrison said it had long been known that older patients don’t do as well in bone marrow transplants as younger ones, and the new finding might explain why.
... The researchers say they do not yet know what stimulus makes cells increase their production of the Ink-4 protein as a person grows older. Their suspicion is that the usual factors implicated in aging, such as mutation and oxidative damage to tissues, would turn out to play a role in making cells produce more Ink-4...
This is not a surprising result. As long as I can remember biologists have suspected that there was a tradeoff between aging rates and cancer.
This seems to fit with the most surprising lay article I've recently read, the discovery that lifespan seems random, that longevity is not hereditable. I'm still fascinated with that result, even though I don't entirely believe it (dogs are my favorite example, there longevity is clearly hereditable and even breed specific). I'm guessing aging rates are hereditable, but they don't translate into longer average lifespan because of the resulting increase in cancer rates (and vice-versa, lower cancer risk doesn't translate into longer lifespan because of faster aging). Still, that's not a complete answer; I think a combination of biological research and simulation modeling will be needed to understand why lifespan is not significantly inherited.
No comments:
Post a Comment