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 all in the end. Except 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 – or at least extended middle age – may be on the horizon.

After discovering two drugs that appeared to invigorate elderly mice, the scientists from Mayo Clinic, the Scripps Institute in Florida and other institutions 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 entirely.

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. The benefits were evident within five days of treatment and lasted for seven months, according to a paper in the journal Aging Cell.

“We view this study as a big first step towards developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders,” says Professor Paul Robbins, who led the research side of the study.

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 says. “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?”

• This article was amended on 2 April 2015. In an earlier version we attributed the study solely to the Scripps Institute. In fact, although the Scripps researchers made major contributions to the study, the first and last authors of the paper are from Mayo Clinic, making it a Mayo study and discovery. We have also clarified that Professor Paul Robbins led the research side of the study, but was not the leader overall; the co-first authors are Tamar Tchkonia and Yi Zhu of Mayo Clinc. The last and senior author is Dr. James Kirkland, head of the Kogod Center on Aging at Mayo Clinic.