Can getting rid of old cells turn back the clock on aging?

Can getting rid of old cells turn back the clock on aging?

Can getting rid of old cells turn back the clock on aging?

James Kirkland began his career in 1982 as a geriatrician, treating aging patients. But he was dissatisfied with what he could offer them.

“I got tired of prescribing wheelchairs, walkers and incontinence devices,” recalls Kirkland, now at the Mayo Clinic in Rochester, Minnesota. He knew that aging is considered the biggest risk factor for chronic disease, but he was frustrated by his inability to do anything about it. So Kirkland went back to school to learn the skills he needed to tackle aging head on, earning a PhD in biochemistry at the University of Toronto. Today, he and his colleague Tamara Tchkonia, a molecular biologist at the Mayo Clinic, are leaders in a growing movement to stop chronic disease by protecting brains and bodies from the biological fallout of aging.

If these researchers are successful, they won’t be short of customers: People are living longer, and the number of Americans 65 and older is expected to double to 80 million by 2040. While researchers like Kirkland don’t expect to extend lifespans, they hope to extend the “health age », the time a person lives free from disease.

One of their targets is waste cells that build up in tissues as people age. These “aging” cells have reached a point—due to injury, stress, or just time—when they stop dividing, but don’t die. While senescent cells usually make up only a small fraction of the total cell population, they made up up to 36 percent of the cells in some organs in aging mice, a study showed. And they don’t just sit still. Aging cells can release a variety of compounds that create a toxic, inflammatory environment that primes tissues for chronic disease. Aging cells have been linked to diabetes, stroke, osteoporosis and several other aging conditions.

These harmful cells, along with the idea that getting rid of them can alleviate chronic diseases and the discomforts of aging, are getting serious attention. The US National Institutes of Health is investing $125 million in a new research effort, called SenNet, which aims to identify and map senescent cells in the human body as well as in mice over the natural lifespan. And the National Institute on Aging has committed more than $3 million over four years to the Translational Geroscience Network multicenter team led by Kirkland that is running preliminary clinical trials of potential antiaging treatments. Drugs that kill aging cells – called senolytics – are among the top candidates. Small-scale trials of these are already underway in people with conditions including Alzheimer’s, osteoarthritis and kidney disease.

“It’s an emerging and incredibly exciting, and perhaps even game-changing, area,” says John Varga, chief of rheumatology at the University of Michigan Medical School in Ann Arbor, who is not part of TGN.

But he and others are also cautious, and some researchers believe the field’s potential has been exaggerated. “There’s a lot of hype,” says Varga. “I have, I would say, a very healthy skepticism.” He warns his patients about the many unknowns and tells them that trying senolytic supplementation on their own can be dangerous.

Scientists are still unraveling the biology of aging cells, not only in aging animals, but also in younger ones—even in embryos, where the aging of certain cells is essential for proper development. So far, evidence that destroying senescent cells helps improve the health span comes mostly from laboratory mice. Only a few preliminary human trials have been completed, with hints of promising but far from blockbuster results.

Still, Kirkland and Tchkonia speculate that senolytics may eventually help not only with aging, but also with conditions suffered by younger people due to injury or medical treatments such as chemotherapy. “There could be applications all over the place,” muses Kirkland.

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