Skip to Content

Drug Reverses ‘Accelerated Aging’ in Human Cells

The discovery has implications for the treatment of several diseases—as well as normal aging in healthy people.

The drug rapamycin has been found to reverse the effects of Hutchinson-Gilford progeria syndrome, a fatal genetic disease that resembles rapid aging, in cells taken from patients with the disease. Rapamycin, an immunosuppressant drug used to prevent rejection of transplanted organs, has already been shown to extend life span in healthy mice. Researchers hope the findings will provide new insight into treating progeria as well as other age-related diseases.

Age reducer: Cells taken from patients with a rapid aging disease were treated with the drug rapamycin. In the top image, a toxic protein called progerin (green) is spread evenly throughout the cells. In the treated cells at bottom, the protein was concentrated and removed much more effectively.

Skin cells from patients with progeria show a slew of defects: deformities in their membranes, decreased growth, and early death. Kan Cao, an associate professor of cell biology and molecular genetics at the University of Maryland, and her colleagues found that rapamycin could reverse these defects by enhancing the cells’ ability to degrade the protein progerin, which accumulates in abnormal amounts in progeria patients. The study was published today in the journal Science Translational Medicine.

It’s not yet clear whether the drug will have similar effects on animals or patients. But progeria researchers are planning a clinical trial of rapamycin. No treatments currently exist for the disease, which is typically fatal by age 12. Children with progeria have health issues typically associated with old age, including balding, hardened skin, pain in joints, hip dislocations, and heart disease.

Researchers say the findings could be relevant beyond this rare genetic disease. Although accumulation of progerin is associated with progeria, the protein also accumulates in small amounts in normal cells, and may be partially responsible for the aging process.

Some age-related diseases, such as Parkinson’s and Alzheimer’s, also result in defects in the cells’ “trash-removal” system, says Dimitri Krainc, associate professor of neurology at Harvard Medical School and one of the authors of the paper. In fact, previous research has shown that the failure of cellular maintenance is a key component of aging. “With normal aging … you start accumulating by-products of normal cell functions,” explains Krainc. Rapamycin may be able to help clean up other toxic proteins as well, though this study only looked at its effects on progerin.

“I would hope that the study increases the search for molecules to replace rapamycin,” which don’t have the immunosuppressant side effects, says David Sinclair, director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School. Such alternatives could be a major step forward in the fight against aging, says Sinclair, who was not involved in the current study.

Keep Reading

Most Popular

A Roomba recorded a woman on the toilet. How did screenshots end up on Facebook?

Robot vacuum companies say your images are safe, but a sprawling global supply chain for data from our devices creates risk.

A startup says it’s begun releasing particles into the atmosphere, in an effort to tweak the climate

Make Sunsets is already attempting to earn revenue for geoengineering, a move likely to provoke widespread criticism.

10 Breakthrough Technologies 2023

Every year, we pick the 10 technologies that matter the most right now. We look for advances that will have a big impact on our lives and break down why they matter.

These exclusive satellite images show that Saudi Arabia’s sci-fi megacity is well underway

Weirdly, any recent work on The Line doesn’t show up on Google Maps. But we got the images anyway.

Stay connected

Illustration by Rose Wong

Get the latest updates from
MIT Technology Review

Discover special offers, top stories, upcoming events, and more.

Thank you for submitting your email!

Explore more newsletters

It looks like something went wrong.

We’re having trouble saving your preferences. Try refreshing this page and updating them one more time. If you continue to get this message, reach out to us at customer-service@technologyreview.com with a list of newsletters you’d like to receive.