With a bit of clever genetic engineering, a team of scientists has just found an astonishing way to significantly expand the natural lifespan of mice. Now, at least one biotech company hopes to translate this breakthrough to fight aging in humans.

In a study published today in the journal Nature, medical researchers at Mayo Clinic College of Medicine—led by cell biologists Darren Baker and Jan van Deursen—have made this decade's biggest breakthrough in understanding the complex world of physical aging. The researchers found that systematically removing a category of living, stagnant cells (ones which can no longer reproduce) extends the lives of otherwise normal mice by 25 percent. Better yet, scouring these cells actually pushed back the process of aging, slowing the onset of various age-related illnesses like cataracts, heart and kidney deterioration, and even tumor formation.

"It's not just that we're making these mice live longer; they're actually stay healthier longer too. That's important, because if you were going to equate this to people, well, you don't want to just extend the years of life that people are miserable or hospitalized," says Baker.

The cells the scientists eliminated are called senescent cells. A senescent cell is an otherwise normal cell—say a skin or heart muscle cell—that has stopped dividing and reproducing. Right now, they're found all over your body. Now, these cells have long been known to be associated with aging, "for example, in mice or people or monkeys, you find an accumulations of these senescent cells over time and with age. And at sites of age-related disease, like osteoporosis, you'll also find these cells," says Baker. One theory behind why these cells exist in the first place is that hyper-stressed cells become senescent to prevent potentially cancerous, unfettered reproduction.

But until now, exactly what effect living senescent cells actually have on the body—either slowing aging, speeding it up, or not effecting the aging process at all—has largely been a mystery. But by leveraging modern techniques in genetic engineering, Baker and his colleagues finally set up an experiment that conclusively proved that the presence of senescent cells is largely a negative one. They shorten total lifespan and hasten the onset of age related illnesses, like cardiovascular disease.

Cellular Kill Switch

Although today's paper is the result of many careful experiments painstakingly developed over a 7 year period, "the beauty of this study is that it's actually really quite simple," says Baker. The scientists took advantage of the fact that one hallmark of senescent cells is that they steadily secrete a certain tumor-suppressing protein molecule called "p16Ink4a." We'll call it p16, and you can think of it as basically their calling card.

By rewriting a tiny portion of the mouse genetic code, Baker and van Deursen's team developed a genetic line of mice with cells that could, under the right circumstances, produce a powerful protein called caspase when they start secreting p16. Caspase acts essentially as a self-destruct button; when it's manufactured in a cell, that cell rapidly dies.

So what exactly are these circumstances where the p16 secreting cells start to create caspase and self-destruct? Well, only in the presence of a specific medicine the scientists could give the mice. With their highly-specific genetic tweak, the scientists had created a drug-initiated killswitch for senescent cells.

In today's paper, Baker and van Deursen's team reported what happened when the researchers turned on that killswitch in middle-aged mice, effectively scrubbing clean the mice of senescent cells. The medicine was injected into the genetically engineered mice's bellies when they were 12 months old. (Keep in mind, the process isn't perfect. Some senescent cells, including those found in the colon and liver managed to survive—possibly by avoiding the killswitch drug.)

The big takeaway is that "we saw about a 25 percent expansion of median lifespan of these mice. This held true for two different genetic strains of mice," each engineered with the killswitch tweak, "and was irrespective of sex or the diet," says Baker. These mice also showed delayed cancer onset, fewer cataracts, an increased drive to explore, and various other age-resistant effects in a wide range of body tissues. The body, it seems, is better off without senescent cells.

As far as the researchers could find, there was pretty much just a single downside of eliminating senescent cells: Wounds healed more slowly. That's no big surprise, as senescent cells are known to play a role in healing and scar-tissue formation.

On To Humans?

Jesús Gil and Dominic Withers, two medical researchers at Imperial College London—who were not involved in today's research—applaud today's research and concur with the results. "The removal of senescent cells does indeed delay ageing and increase healthy lifespan," they write in an essay accompanied alongside the research paper in the journal Nature.

So what's next? Well, at the same time today's paper was published, a company called Unity Biotechnology launched, with the stated goal to use today's breakthrough understanding of senescent cells to develop medicines that fight the process of aging. (Obviously they're going to have to use a different approach to genetically engineering humans.)

"Imagine drugs that could prevent and maybe even cure arthritis or heart disease or loss of eyesight. It's an incredible aspiration," said Nathaniel David, Ph.D., CEO of Unity Biotechnology in a press release. "If we can translate this biology into medicines, our children might grow up in a different world than we did. There will be many obstacles to overcome, but our team is committed and inspired to achieve our mission."

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