Could the effects of aging be delayed or even prevented simply by clearing the body of old cells? Scientists report in Nature that they were able to do just that in a study of mice.
It is the first study to show that when senescent cells — those that have gotten old and stopped dividing — build up, they can promote aging in nearby tissues, contributing to such age-related conditions as cataracts, skin wrinkling and muscle loss. Senescent cells are few in number, but their effects may be wide-ranging.
Normally, these old cells are cleared by the body, but the process becomes less efficient with age. So researchers at the Mayo Clinic used a drug to target only senescent cells and force them to self-destruct in a group of mice that were genetically engineered to age rapidly.
In mice that were treated throughout their lifetimes, researchers said they saw a remarkable delay in the development of cataracts, muscle wasting and the type of fat loss that, in humans, causes skin wrinkling. Another group of mice was treated in older age, after cataracts had already set in. The drug didn’t reverse the age-related changes that had already occurred, but it prevented further decline.
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The importance of cell senescence to the aging process has long been suspected. But the latest finding demonstrates definitively that these cells play a role in age-related conditions, according to Felipe Sierra, director of the division of aging biology at the National Institute on Aging, who wasn’t involved in the study.
When cells become senescent, they produce harmful compounds such as those that cause inflammation. Chronic tissue inflammation with aging is thought to underlie dementia, atherosclerosis and diabetes, among other ills, according to James Kirkland, head of Mayo’s Center on Aging, who was also an author of the study.
The key question for further research is whether the same antiaging effects could be seen in people. Senescence is thought to have developed as a protection against cancer, which is caused by cells that divide uncontrollably, so curbing that mechanism would be risky. But perhaps drugs can be developed to target senescent cells and clear them from the body altogether, or destroy the inflammatory compounds these cells produce.
The study offers numerous avenues for future research. It’s not clear, for instance, how often or how many senescent cells would have to be eliminated to have an effect. It’s also unknown whether senescent cells have different effects in different tissues of the body.
The Mayo Clinic researchers plan to repeat their experiment with normal mice, which have not been engineered to age prematurely, to see whether the treatment has an influence on longevity. In the current study, the cell-clearing drug had no effect on lifespan, since the animals were bred to have heart attacks and die at an early age.
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Ultimately, however, the point of such investigation is not to seek ways to stop aging, but rather to maintain health into old age. “If you attack the fundamental aging process, can you attack age-related illnesses as a whole?” Kirkland asked in an interview with HealthDay. “Can you delay cancer, dementias, atherosclerosis, diabetes, obesity and its complications as a group?”