Senescent Cells Contribute to Aging. Recent Study Finds a Way To Stop Them!
There is a way to slow down the aging process. Stop the Zombies, those senescent cells that cause inflammation, cataracts, add plaque to your arteries and exacerbate the flabby skin, creaks and pain in your joints. The Mayo Clinic in Rochester Minnesota, may have discovered one of the most beneficial results to encourage the "Youth Movement!"
Their new study shows that researchers have actually purged mice bodies of senescent cells. And with the purging, goes the attenuating effects of age, slowing the process down measurably. But hold on. You know what's coming next. More research has to be done. We don't want to make crude and cruel assumptions that tomorrow, we can swallow a "fountain of youth" pill. (Nicholas Wade, The New York Times)
The research team headed by Darren J. Baker and Jan M. van Deursen genetically engineered a mouse in which all the senescent cells could be eradicated when administered a drug that causes the cells to self-destruct. Researchers reported online Wednesday in the journal Nature, that the mice tissues showed a significant improvement in the usual list of age-related disorders. They did not develop cataracts. Their muscle tissue remained strong, not wasted. And exercising on the mouse treadmill was a breeze, as they exercised for a much longer period. Mouse flab? The subcutaneous fat layers that keep the healthy, youthful mouse look were retained. With age, those fat layers drain away the bloom and shrink, a major cause of wrinkling. (David W. Freeman, CBS News)
From a study conducted years ago, scientists have known that cell division doesn't continue but instead, cells reach a static state of "cellular senescence," releasing substances that damage adjacent cells and cause inflammation. The immune system normally sweeps away these accumulating "living-dead" cells, but gradually loses its ability to do so. (CBS News)
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After finding that such cells "reliably switch on a characteristic marker gene known as p16-Ink4a," van Deursen engineered the genetic element that switches on the marker gene to kick in a mechanism to make the cell self-destruct. He found that the mechanism triggered when the mice were treated with a specific drug, resulting in the condition that senescent cells, vulnerable to the drug, could be purged at any manipulated point in the mouse’s lifetime. (Nicholas Wade, The New York Times)