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June 24, 2025

Researchers discover how caffeine could slow cellular aging

Fission yeast cells in which the glucose transporter Ght5 is fluorescently labeled with green fluorescent protein (GFP). Credit: Olga Xintarakou, Queen Mary University of London
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Fission yeast cells in which the glucose transporter Ght5 is fluorescently labeled with green fluorescent protein (GFP). Credit: Olga Xintarakou, Queen Mary University of London

A new study from the Cellular Aging and Senescence laboratory at Queen Mary University of London's Centre for Molecular Cell Biology reveals how caffeine—the world's most popular neuroactive compound—might do more than just wake you up.

in the journal Microbial Cell shows how could play a role in slowing down the at a cellular level.

Caffeine has long been linked to potential health benefits, including reduced risk of age-related diseases. But how it works inside our cells, and what its exact connections are with nutrient and stress-responsive gene and protein networks, has remained a mystery—until now.

In new research published by scientists studying —a single-celled organism surprisingly similar to —researchers found that caffeine affects aging by tapping into an ancient cellular energy system.

A few years ago, the same research team found that caffeine helps cells live longer by acting on a growth regulator called . TOR is a biological switch that tells cells when to grow, based on how much food and energy is available. This switch has been controlling energy and stress responses in living things for over 500 million years.

But in their latest study, the scientists made a surprising discovery: Caffeine doesn't act on this growth switch directly. Instead, it works by activating another important system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

How caffeine affects cells. Credit: Queen Mary University of London
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How caffeine affects cells. Credit: Queen Mary University of London

"When your cells are low on energy, AMPK kicks in to help them cope," explains Dr. Charalampos (Babis) Rallis, Reader in Genetics, Genomics and Fundamental Cell Biology at Queen Mary University of London, the study's senior author. "And our results show that caffeine helps flip that switch."

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Interestingly, AMPK is also the target of metformin, a common diabetes drug that's being studied for its potential to extend human lifespan together with rapamycin.

Using their yeast model, the researchers showed that caffeine's effect on AMPK influences how cells grow, repair their DNA, and respond to stress—all of which are tied to aging and disease.

"These findings help explain why caffeine might be beneficial for health and longevity," said Dr. John-Patrick Alao, the postdoctoral research scientist leading this study. "And they open up exciting possibilities for future research into how we might trigger these effects more directly—with diet, lifestyle, or new medicines."

So, the next time you reach for your coffee, you might be doing more than just boosting your focus—you could also be giving your cells a helping hand.

More information: John-Patrick Alao et al, Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast, Microbial Cell (2025).

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Caffeine slows cellular aging by activating AMPK, a conserved energy sensor in cells, rather than acting directly on the TOR growth regulator. This activation influences cell growth, DNA repair, and stress responses, processes linked to aging and disease, suggesting a molecular basis for caffeine’s potential health and longevity benefits.

This summary was automatically generated using LLM.