The scientists used p16 to activate a type of "suicide gene" within senescent cells. The protein made by this gene will kill senescent cells (without harming other normal cells) after a drug specifically designed to activate it is administered, said van Deursen.
Two sets of prematurely aged mice were involved. In one set, the researchers cleared senescent cells for the whole 15 months of the mice's typical lifespan. In another set of mice, they waited until age-related problems were well underway and then cleared the senescent cells away for a few months, said Kirkland.
The result: Lifelong destruction of a mouse's senescent cells kept age-related problems at bay, including cataracts and loss of muscle mass and strength. But the study also suggested that removing senescent cells later in life could slow down these age-related health problems.
What's more, said Kirkland, improved behavior was noted -- the activity level of the mice was considerably higher.
Still, the research is early and has not yet moved into experiments in humans. "It's a proof of principle study. Now we know we can safely remove these cells in an animal model without causing any detectable harm," said van Deursen.
Dr. Gary Kennedy, director of the Division of Geriatric Psychiatry at Montefiore Medical Center in the Bronx, and an expert in aging, said the work was exciting.
"When they blocked the senescent cell process in mice prone to premature aging, they blocked the development of spinal arthritis, the loss of muscle, thinning of skin -- they were all reversed. Mice that should have looked prematurely aged were essentially normal," Kennedy noted. But he stressed that the research needs to be replicated in other species as well before the public gets excited about its medical promise.
"I thought it was a very interesting paper. I was actually surprised by the data -- no one else has been able to do this," added Dr. Ju
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