It sounds like science fiction. Scientists take ordinary skin or blood cells, rewind them to a stem-cell state, then reprogram them into a kind of youthful immune cell. They then inject these into an aging or Alzheimer’s-stricken mouse and those cells sharpen memory, calm brain inflammation, and even make neurons look younger. Yep, totally sci-fi.
Except it’s real. Just in mice, for now, but promising for humans as well.
A new study from Cedars-Sinai Medical Center is promoting this bold way to treat Alzheimer’s and other brain ailments. And it all starts with an unlikely hero: a type of white blood cell called a mononuclear phagocyte.
No “Blood of the Young” Needed
Scientists have long been fascinated by the rejuvenating powers of “young blood.” More than two decades ago, experiments showed that transfusing blood plasma from young mice into old ones boosted memory and learning. Bone marrow transplants from younger animals worked too.
But there are big problems with that approach. First of all, there’s the big and very obvious ethical problem with that. The prospect of harvesting blood and marrow from children is as dystopian as it gets. Secondly, even if you overcome the ethical problem, these approaches don’t scale. Plasma from the young is limited and bone marrow transplants are invasive and risky.
“Previous studies have shown that transfusions of blood or plasma from young mice improved cognitive decline in older mice, but that is difficult to translate into a therapy,” said Clive Svendsen, PhD, executive director of the Board of Governors Regenerative Medicine Institute and senior author of the study. “Our approach was to use young immune cells that we can manufacture in the lab — and we found that they have beneficial effects in both aging mice and mouse models of Alzheimer’s disease.”
Svendsen and colleagues used induced pluripotent stem cells (iPSCs), adult cells that can be reprogrammed into any other cell type. They turned these stem cells into fresh batches of youthful mononuclear phagocytes, which they call iMPs.
These iMPs act like “janitors,” cleaning debris from the body and fighting infection. In time, they can become less effective. Over three weeks, the scientists injected iMPs into the animals’ veins. The cells didn’t migrate to the brain. Instead, they lodged in peripheral organs like the lungs and spleen, which was initially considered disappointing — except the results were startling.
The treated mice performed better on memory tests, especially those requiring the hippocampus, the brain’s memory hub. They recognized objects and remembered spatial layouts almost as well as youthful mice. When the researchers peered inside the hippocampus, they saw rejuvenated mossy cells — neurons critical for encoding new experiences. Even more intriguing, some of the genetic signatures of aging itself seemed to be disappearing.
Fighting Both Aging and Alzheimer’s
If the cells never reached the brain, how did they work their magic? The answer seems to lie in the bloodstream.
Researchers looked at the proteins of mouse plasma, which showed the iMPs reversed several aging-related changes. Most strikingly, they lowered levels of serum amyloid proteins, a family of proteins primarily synthesized in the liver that play a key role in the body’s response to inflammation and infection. In lab dishes, these proteins killed human microglia. But when the same toxic proteins were paired with iMP-conditioned media, the microglia survived.
In short, the cells seemed to act less as janitors and more as remote bodyguards: parked in peripheral organs, releasing factors into the blood that shield the brain from afar.
The scientists didn’t stop with normal aging. They also tested iMPs in mice suffering from a model of Alzheimer’s disease. They observed a preventive effect, even in mice that already had severe symptoms. Their spatial memory improved, and they seemed to have healthier brain activity.
But here’s the twist: iMPs didn’t reduce the classic Alzheimer’s plaques. The therapy improved cognition without sweeping away amyloid. That suggests Alzheimer’s damage is about more than plaques, and that tamping down inflammation and protecting neurons may matter just as much.
Can It Work for humans?
Let’s not get ahead of ourselves. The caveats, for now, are very real. These results come from mice, not people. Human brains and immune systems are far more complex and stem-cell therapies carry risks, from immune rejection to runaway growth. The Cedars-Sinai team admit even they still doesn’t fully understand which factors secreted by iMPs are doing the heavy lifting.
Clinical translation will require years of safety studies, careful dosing trials, and ethical oversight. As with any promising Alzheimer’s therapy, there’s an entire graveyard of once-hyped ideas that fizzled in human trials.
Yet, the fact that iMPs worked in multiple mouse models, across both aging and Alzheimer’s, is unusual — and encouraging.
Alzheimer’s is a looming crisis. More than 55 million people worldwide live with dementia, and Alzheimer’s accounts for up to 70 percent of those cases. Drugs targeting amyloid have dominated the field for decades, yet their benefits remain modest and controversial. This study promises a new, radically different approach. If it works in humans, it could open a new chapter in dementia therapy.
Even beyond Alzheimer’s, the implications are vast. Normal cognitive decline with age — misplacing names, losing sharpness — affects hundreds of millions. A therapy that keeps the brain young without major surgery or scarce donor material could be transformative.
In the meantime, the study injects new energy into a field hungry for breakthroughs. It shows that rejuvenation isn’t just a metaphor. With the right kind of engineered cells, you really can make an old brain act young again — at least in mice.
The study was published in Advanced Science
