Scientists in the UK have moved a step closer to understanding how ageing might be slowed after creating a drug that extended the lives of several animals.
The experimental compound, known as 991, increased the lifespan of yeast, worms and flies by as much as 25 per cent.
The drug activates AMPK, a protein that helps cells preserve and generate energy during periods of stress, exercise or fasting. Researchers have long believed that this natural survival response could also delay some of the biological processes linked to ageing.
The findings raise the possibility that the same approach could eventually benefit humans, although scientists stress that much more research is needed.
Professor Filipe Cabreiro, of the UK’s Medical Research Council (MRC), said: ‘The field is still a long way from anti-ageing clinical trials in humans. This is because ageing is not technically classified as a disease.
‘But improving health in older age would be hugely beneficial from a societal and healthcare perspective, since ageing is a major risk factor for so many diseases, such as heart disease, diabetes, cancer and dementia.
‘The ability to make individuals healthier for longer, for instance by pharmacologically targeting energy balance through AMPK, would be a major biomedical breakthrough.’
The study found that the experimental drug extended the lifespan of yeast, worms and flies by up to 25 per cent
AMPK is often called the body’s ‘fuel gauge’ because it continuously monitors the amount of energy available inside cells.
When energy supplies decline, AMPK functions as a biological switch. It suppresses processes that consume large amounts of energy while activating systems that produce more fuel.
Exercise, fasting and other forms of physical stress naturally stimulate the enzyme, allowing cells to adapt when resources are scarce.
Interest in AMPK has grown because the protein affects several processes associated with ageing, including metabolism, inflammation and cellular repair.
As a central part of the body’s metabolic network, AMPK has also been connected with conditions such as obesity, type 2 diabetes, cardiovascular disease and dementia.
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Some widely used medicines, including the diabetes drug metformin, are known to activate AMPK. This has prompted researchers to investigate whether the pathway could be used to support healthier ageing.
However, many of these medicines activate AMPK indirectly, which makes their biological effects more difficult to establish and interpret in both laboratory studies and clinical research.
The experimental drug 991 activates AMPK, a protein that regulates energy levels inside the body
To address this limitation, the researchers used 991 to activate AMPK directly in fission yeast, nematode worms and fruit flies.
These organisms were selected because their relatively short lifespans allow scientists to study the effects of potential anti-ageing treatments more quickly.
Dr Helena Cochemé, who leads the Redox Metabolism Group at the MRC, said: ‘The fact that we can extend lifespan in yeast, worms and flies is very exciting.
‘Worms and flies in the lab live for around three weeks and three months respectively, …so we can make progress and discoveries much more rapidly and efficiently than in mammalian systems.
‘Our study is the first demonstration that directly targeting AMPK using a drug can have longevity benefits in living organisms.
‘If a treatment works successfully in three such distantly related species, then these results give us more confidence that in the longer-term, the effects possibly translate to mammals and eventually perhaps humans.’
Having demonstrated clear longevity benefits in yeast, worms and flies, the scientists are now aiming to see whether the same effects can be replicated in mice.
They say the fact that direct AMPK activators have already shown a good safety profile in trials for metabolic conditions raises hopes that the drugs could one day be used more widely in medicine.
The study, published in the journal Aging Cell, was primarily publicly funded by the MRC, part of UKRI.
The research also involved contributions from scientists at Queen Mary University of London, the Francis Crick Institute and the University of Lyon.