Fascinating picture shows anti-ageing drugs really DO work: One mouse given the medication kept its glossy brown fur – while another untreated mouse started to go grey
- Mice treated with the drugs kept their glossy fur and bright eyes
- Stark contrast to the frail, tired-looking mice who did not receive the medication
- Drugs extended the rodents’ lifespan by 36% – equivalent of 30 human years
- Six trials are testing the drugs in humans, which may be available in two years
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A fascinating picture of two very different mice shows anti-ageing drugs really do work.
Scientists gave the youth-enhancing medication to mice, with some of the rodents being left with glossy fur and bright eyes.
This is a stark contrast from the frail, tired-looking mice who did not receive the drugs – and could easily be confused as being twice as old as the treated animals.
Researchers found giving the rodents anti-ageing – or senolytic – drugs extended their lives by 36 per cent – the equivalent of around 30 human years.
Six trials testing senolytic drugs in humans are already underway and a further half a dozen are due to start in the near future.
Scientists gave the youth-enhancing medication to mice, with some of the rodents being left with glossy fur and bright eyes (right). This is a stark contrast from the frail, tired-looking mice (left) who did not receive the drugs – and could easily be confused as being twice as old as the treated animals
If successful, medication that slows ageing may be available in as little as two years, the researchers claim.
The research was carried out by the Mayo Clinic in Rochester, Minnesota, and led by Dr James Kirkland, a clinical geriatrician and director of the Robert and Arlene Kogod Center on Aging.
‘Most people don’t want to live to 130 and feel like they’re 130 but they wouldn’t mind living to 90 or 100 and feel like they’re 60,’ Dr Kirland told The Telegraph.
‘And now that can actually be achieved in animals.’
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Ageing is thought to play a role in the onset of everything from cancer and arthritis to Alzheimer’s and heart disease.
Dr Kirkland notes it is very rare for a person to suffer from just one chronic age-related disease, with most people battling several conditions at once.
This suggests there is a common mechanism behind ‘old people’ disorders.
‘You tend to find older individuals who are completely healthy and are playing 18 rounds of golf a day, or they’ve got three, five or ten different conditions,’ Dr Kirkland said.
Pictured left, the untreated mouse, compared to the mouse that did receive the drugs, right
WHAT ARE SENESCENT – OR ‘ZOMBIE’ – CELLS?
Senescent – or ‘zombie’ – cells are formed from normal cells but have lost the ability to divide.
These cells are ‘alive’ but non-functioning and do not get cleared away as normal by the body.
Otherwise healthy cells are thought to age due to the accumulation of senescent cells, which may trigger inflammation or release harmful chemicals.
Although senescent cells accumulate with age, they are thought to only become dangerous once they reach a critical threshold.
They likely come about themselves due to DNA damage or inflammation, as well as an inability to turn genes ‘on and off’ at the correct time.
Perhaps most importantly, senescent cells have been found to cluster around the lesions of heart-attack patients, the bones of osteoporosis sufferers and the joints of those with arthritis.
And transplanting organs from older patients into younger people has been found to raise the latter’s risk of age-related diseases.
The transferal of senescent cells is thought to be to blame.
Rather than just trying to treat one disease, scientists are now looking to create a broad-spectrum drug that can ‘turn off’ the process that triggers a host of conditions.
Dr Kirkland compares this to an antibiotic that is capable of relieving up to 25 infections.
He argues it is always better to treat the mechanism behind a disorder rather than just masking its symptoms.
Dr Kirkland added he is ‘tired’ of prescribing wheelchairs and incontinence products to older people, and believes ‘disease modifying’ interventions are critically needed.
Senolytic drugs target senescent – or ‘zombie’ – cells, which have lost the ability to divide.
These cells are ‘alive’ but non-functioning and do not get cleared away as normal by the body.
Otherwise healthy cells are thought to age due to the accumulation of senescent cells, which may trigger inflammation or release harmful chemicals.
Although senescent cells accumulate with age, they are thought to only become dangerous once they reach a critical threshold.
They likely come about themselves due to DNA damage or inflammation, as well as an inability to turn genes ‘on and off’ at the correct time.
Perhaps most importantly, senescent cells have been found to cluster around the lesions of heart-attack patients, the bones of osteoporosis sufferers and the joints of those with arthritis.
And transplanting organs from older patients into younger people has been found to raise the latter’s risk of age-related diseases.
The transferal of senescent cells is thought to be to blame.
Ageing is thought to play a role in the onset of everything from cancer and arthritis to Alzheimer’s and heart disease. Six trials testing senolytic drugs in humans are underway, with researchers being ‘optimistic’ the medication may be available in as little as two years (stock)
The mice in the Mayo study were given a senolytic-drug cocktail of dasatinib, which is usually used to treat leukemia, and the plant-supplement quercetin, which is found in green tea, red wine and apples.
When other scientists have transplanted senescent cells into young animals, the animals have then shown signs of ageing and developed related diseases.
But administering senolytic drugs clears these senescent cells away by triggering their ‘suicide’ and shutting down their energy supply.
And the cells are then replaced with healthy tissue.
A study also found exposing tissue taken from obese diabetic patients to senolytic drugs caused their fat cells to respond to insulin again.
But before senolytic drugs can be prescribed, they must first be tested in human trials.
Six trials are already underway and a further half a dozen more are due to start in the near future.
One was carried out on 14 older patients with idiopathic pulmonary fibrosis, which causes the lungs to become scarred and makes breathing difficult.
Results revealed just nine doses of the drugs over three months improved the patients’ walking speed and how far they could move, as well as reducing their frailty.
Dr Kirkland called the results ‘highly significant and dramatic’, with most idiopathic pulmonary fibrosis patients never experiencing any improvement.
The findings motivated his team to carry out a larger study on patients who ‘wouldn’t have that much to lose if something went wrong’.
Reassuringly, all the mice involved in the more recent Mayo study remained in good health.
If studies continue to be successful, the scientists may start looking at how senolytic drugs benefit those with more minor conditions, such as mild cognitive impairment, frailty and incontinence.
Dr Tamara Tchkonia – who works with Dr Kirkland – claims senolytic drugs could be available in the next two years, but admits she is an ‘optimistic person’.
The Mayo Clinic has joined up with seven other research institutions across the US to form the Translational Geroscience Network, which will carry out the studies.
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