New range of drugs may slow ageing process by taking out 'senescent' cells
New drugs reinvigorated elderly mice by removing 'senescent' cells that build up over time and accelerate ageing process
It is generally accepted as one of life's unfortunate but inevitable facts: we might be able to disguise the wrinkles for a time, but ageing will get us in the end.
But scientists are now questioning whether it has to be thus, or whether age is simply another disease that might one day be conquered. American researchers have suggested that the elixir of eternal youth may be on the horizon.
After discovering two drugs that appeared to invigorate elderly mice, the scientists, from the Scripps Institute in Florida, have coined the term "senolytics" for a new class of drugs designed to delay the ageing process. Their research focuses on so-called senescent cells - cells we acquire throughout life that shut down, stop dividing and sit there making few useful contributions to our lives.
"Senescence used to be thought of as an inert state," says Sian Henson, a specialist in ageing at University College London.
"But we now know they make a whole load of things that are bad for you. They're definitely trouble."
The older we get, the more of these cells we have. As they sit in our tissues pumping out harmful inflammatory molecules, they trigger senescence in neighbouring cells, accelerating the ageing process. The logical solution, the Scripps team reasoned, would be to get rid of senescent cells.
In a study in mice, they found that two licensed drugs were effective at eliminating these cells from fat tissue and bone marrow.
When the mice were given the cancer drug dasatinib (targeting fat) and the antihistamine quercetin (bone marrow), they had improved cardiovascular function, better stamina, reduced osteoporosis and frailty, and extended healthy lifespan.
Benefits were evident within five days of treatment and lasted seven months, according to a paper in the journal .
Henson agrees that the approach roughly makes sense, but says it will be some time before senolytics are available on prescription.
"Overall, what they're doing is sensible," she said. "Would I want to take what they gave to the mice? I don't think so."
A central drawback, she points out, is that unless you replace senescent cells with healthy versions, "you'd actually shrink a bit".
After a few rounds of treatment, the process would presumably become unsustainable.
A promising alternative to drugs, Henson says, would be to harness the body's own immune system to sweep out senescent cells more gradually, giving the body time to replace them. Preliminary work suggests that T-cells, which normally target disease, can be genetically engineered to target senescent cells in a wide range of tissues.
In future, an infusion of GM blood every few years might be able to keep you going indefinitely (assuming some major advances in treating cancer, Alzheimer's and heart disease). At which point, the question might be less: 'How long have I got?' and more: 'How long do you fancy sticking around?'
