Here’s what you’ll learn when you read this story:

• A scientist wants to reprogram cells so they regain a more youthful state while maintaining their normal function.
• If we treat aging like we do disease, we could learn how to maintain biological function and keep people’s body parts younger, some researchers hope.
• However, some think that’s not yet possible without causing unintended side effects, and the safety margin for how to reprogram cells is still not determined.

In The Curious Case of Benjamin Button, a Hollywood blockbuster set in 20th-century America, we watch Benjamin Button enter the world with the body of an 80-year-old man, only to age in reverse. The symbolism is hard to miss: after reliving the fruits of youth, he still fades into infancy, a subtle reminder of the hubris of trying to defy nature.

And yet, for Yuri Deigin, cofounder of Seattle-based YouthBio Therapeutics, where Hollywood gets it wrong is simple: you can’t make an 80-year-old suddenly become 20 years old. Reverse aging is not a cataclysmic whole-body reset. “It will first mean restoring more youthful function to specific cells, tissues, and organs,” he says.

And that’s Deigin’s goal: to reprogram cells so they regain a more youthful state without losing what makes them what they are. He does not imagine a sudden reversal of aging across the whole body, but rather a gradual process that begins in specific tissues and builds over time. Early versions of these therapies, he says, could begin to emerge within the next decade. If they work, the stakes are not cosmetic. They would change how we treat disease, shifting medicine toward maintaining biological function itself.

The idea rests on a deceptively simple premise: aging is not simply damage, but a program. “My view is that the epigenome [the set of chemical switches that control how genes are turned on and off] is the closest thing biology has to a writable operating system that helps determine cellular age,” Deigin says. As cells grow older, this epigenome drifts, becomes noisier, and loses some of its precision. The goal of what scientists call partial cellular reprogramming is to reset that system, pushing cells back toward a younger, more functional state without erasing their identity.

There are, broadly speaking, two ways to reprogram a cell. One—full reprogramming—is the more mind-bending, almost sci-fi version, loosely reminiscent of what might be happening to Mr. Button. It involves resetting an adult cell into an embryonic-like state. The second, partial reprogramming—the approach Deigin is betting on—is less extreme. It builds on a set of genes known as the Yamanaka factors, which are powerful regulators that can reset a cell’s biological clock by changing its gene expression patterns. But instead of fully activating the Yamanaka factors, researchers are trying to pulse them just enough to restore function without wiping their identity. In practice, that means delivering the genes that encode these factors into specific (aging) organs, and activating them in controlled bursts, potentially through periodic activation.

YouthBio’s lead program, called YB002, targets the brain, with a focus on Alzheimer’s disease. In preclinical studies, including models of cognitive decline, the therapy has shown early signs of activity. More recently, the company received feedback from the U.S. Food and Drug Administration (FDA) supporting its proof of concept, and now has plans for a first-in-human trial. For Deigin, that progress is only the beginning.

Rejuvenation, he says, will likely unfold piece by piece.

“One therapy may rejuvenate the eye. Another may target the brain, heart, immune system, liver, or muscle.” Only later, he adds, might those approaches be combined into something broader. “True whole-body rejuvenation will likely require a combination of tissue-specific therapies,” he says—in other words, there is no modern fountain of youth.

One of the clearest examples emerging from this step-by-step approach is in the eye.

At Boston biotech company Life Biosciences, researchers are testing an approach that aims to coax damaged optic nerve cells back into a more youthful state. In animal studies, it has improved aspects of vision after injury and pushed cells toward younger patterns of function, says Sharon Rosenzweig-Lipson, PhD, the company’s chief scientific officer. The work has now moved into an early human trial, where the company is testing its lead therapy, ER-100, in people with optic nerve damage. For now, the goal is modest: to see if some of that lost function can be restored safely. “Near term, these therapies have the potential to restore function in specific tissues that are impacted by aging,” she says.

The eye may be more straightforward. But what about the brain and its complexity, the “seat of personality,” with all those questions of memory and consciousness surrounding it?

Deigin believes that concern reflects a deeper misunderstanding. The goal is not to erase who we are, but to support it. “The ideal therapy would rejuvenate the biological machinery of the neuron while preserving the informational content of the network,” he says. In simpler terms: make the hardware younger without scrubbing the software. Early animal work points in that direction, he says, suggesting that partial reprogramming in the brain can actually improve memory performance rather than expunge it. “That is not proof that this will work safely in humans, but it is very encouraging,” Deigin says.

Others are more cautious.

“Once neuron loss occurs, it would be hard to rejuvenate,” says Koji Tanabe, PhD, a stem cell scientist and CEO of I Peace, a gene therapy company in Palo Alto, California. He worked with Shinya Yamanaka, the researcher whose name now defines the reprogramming factors. As the brain ages, neurons become more fragile, and once they are gone, they are not easily replaced. Keeping existing cells healthy may be within reach. Rebuilding what is lost is not within reach—at least not yet, notes Tanabe.

There is also a deeper misconception, Tanabe continues, that partial reprogramming is the same as reversing aging. In the lab, “reprogramming” usually means something quite drastic: reconfiguring the cell’s identity. “Reverse aging,” by contrast, is closer to regaining youthful function while preserving that identity, he notes.

That’s why Deigin says they are careful about how far to push the reprogramming process. Full reprogramming would overwrite a cell’s identity: you would essentially turn a skin cell into a stem cell. In the brain, that would be disastrous. But partial reprogramming tries to stay on the safe side of that line. The idea is to nudge cells toward a younger state without changing what they are, by switching those factors on briefly and under control, Deigin says.

The brain may also have a small advantage. Neurons are unusually stable cells that rarely divide, which may make them less prone to losing their identity than more active tissues. “That does not eliminate the risk, but it may provide a larger safety window than you would have in tissues such as the liver or intestine, where cells are naturally more proliferative,” Deigin says.

But that safety margin is exactly what researchers are still trying to define. In 2026, no therapy aimed at reversing aging has been approved by the FDA, and earlier studies herald caution. A study in Nature found that inducing reprogramming factors in living mice could lead to teratomas, tumors made up of different types of tissue, such as hair, muscle, or bone. Earlier, a study published inCell showed that even partially reprogrammed cells, if pushed or interrupted at the wrong moment, could become dysplastic and form cancer-like growths across multiple organs. Together, these findings highlight the core problem: not just how far to rewind the system, but how precisely to control it.

That uncertainty shapes how regulators see the field. Rosenzweig-Lipson expects a step-by-step path, with treatments approved one condition at a time. Deigin also accepts that trajectory as the likely path. “The first approvals will almost certainly come disease by disease—Alzheimer’s, glaucoma, heart failure, sarcopenia, immune aging, and so on,” he says. At the same time, he argues that the medical establishment is missing the forest for the trees, treating conditions separately in what he calls reactive disease treatment. If instead medicine adopted a more proactive maintenance of biological function, it would change how we treat disease altogether.

“We would stop seeing aging as an inevitable one-way decline and start seeing it as a modifiable biological state,” Deigin says, a shift that could mark one of the most profound transitions in human history.

Some skeptics would certainly recoil at hearing this. They see these efforts as a techno-utopian bid to erase the sense of direction and purpose built into life, replacing it with a project of indefinite maintenance. If our lives just keep going, the eventual endpoint raises serious questions about whom we would make room for on a planet with finite resources.

Deigin pushes back. For him, the real moral failure is simpler: “Aging causes enormous suffering,” he says. “Such a shift would reshape retirement, careers, healthcare, family planning, and even our assumptions about human potential.”

If reversing cellular aging becomes a reality, then perhaps we would all become a sort of Benjamin Button, only without the fantasy—and without the tragedy.