Summary: New research from Queen Mary University of London suggests caffeine may slow cellular ageing by activating AMPK, an evolutionarily conserved energy-sensing pathway. Using fission yeast as a model for human cells, scientists found that caffeine increases AMPK activity, which helps cells manage energy stress, repair DNA, and regulate growth—processes closely linked to ageing and age-related disease risk.
AMPK is a central regulator of cellular energy balance and is also a pharmacological target of metformin, a widely used diabetes drug that is being investigated for potential lifespan and healthspan benefits. These findings shed light on how caffeine interacts with ancient cellular systems that protect against age-related damage.
Key Facts:
- AMPK activation: Caffeine enhances AMPK, a cellular “fuel gauge” associated with stress response and longevity-related pathways.
- Deep evolutionary roots: The energy-stress network influenced by caffeine is conserved across species and is more than 500 million years old.
- Yeast model insights: Experiments in fission yeast reveal molecular mechanisms that are likely conserved in human cells and useful for studying ageing.
Source: Queen Mary’s University of London
A team at the Cellular Ageing and Senescence Laboratory within Queen Mary University of London’s Centre for Molecular Cell Biology has published new work describing how caffeine — the world’s most widely consumed psychoactive compound — can influence cellular pathways tied to ageing.
Caffeine has long been linked in epidemiological studies to a lower risk of some age-related diseases and to certain health benefits, but the precise molecular connections inside cells remained unclear. To explore those connections, researchers turned to fission yeast, a single-celled organism whose basic cell biology is remarkably similar to that of human cells and which is commonly used to understand conserved pathways involved in growth, stress response, DNA repair, and ageing.
Earlier work from this group showed that caffeine can extend cellular lifespan by affecting the TOR (Target of Rapamycin) pathway, a major growth regulator that coordinates cell growth with nutrient availability. TOR has been a focus of ageing research because it influences how organisms allocate resources for growth versus maintenance and repair.
In the new study, researchers discovered that caffeine does not primarily act on TOR itself but instead activates AMPK, a complementary energy sensor. AMPK becomes active when cellular energy levels are low and shifts cell behaviour toward energy conservation and maintenance activities. By boosting AMPK activity, caffeine appears to promote processes that help cells cope with stress, repair DNA damage, and restrain inappropriate growth—mechanisms that collectively support cellular health and may slow aspects of cellular ageing.
“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 and the study’s senior author. “Our results show that caffeine helps flip that switch, engaging conserved energy and stress-response programs.”
Dr John-Patrick Alao, the postdoctoral scientist who led the experimental work, adds that these findings offer a clearer molecular explanation for some of the beneficial associations seen with caffeine consumption and open avenues for further research into targeted interventions—whether through diet, lifestyle, or new compounds—that could mimic or enhance these protective cellular responses.
Because AMPK is also targeted by metformin, a drug already under investigation for its potential to improve healthspan, the new results help place caffeine within a broader framework of interventions that act on evolutionarily conserved metabolic regulators. The study does not claim caffeine is a proven anti-ageing therapy in humans, but it provides robust cellular-level evidence that may guide future studies in more complex organisms.
These findings underscore the value of model organisms in ageing research and highlight how common dietary compounds can influence fundamental cellular systems. They also invite carefully designed follow-up studies to determine how these cellular effects translate into whole-organism outcomes and what role lifestyle or pharmacological strategies might play in promoting healthy ageing.
About this genetics and aging research news
Author: Lucia Graves
Source: Queen Mary’s University of London
Contact: Lucia Graves – Queen Mary’s University of London
Image: The image is credited to Neuroscience News
Original Research: The study will appear in the journal Microbial Cell.