Research into longevity, that most fundamental and intractable of all human health challenges, is slow moving. It deserves to be described in terms of years, not individual studies. But once in a rare while, a finding has the potential to be a landmark.
Such is the case with a new experiment that flushed old, broken-down cells from the bodies of mice, slowing their descent into the infirmities of age.
The usual caveats that inevitably apply to mouse studies still apply here. But even with those, the findings mark the first time that cellular senescence — its importance debated by biologists for decades — has been experimentally manipulated in an animal, demonstrating a fantastic new tool for studying its role in human aging.
And even if the results are applicable only to one strain of genetically modified mice, it’s hard to not at least notice what happened to them. Already programmed to die from heart disease, they didn’t live longer than usual, but they were far healthier.
“Their healthspan was extended,” said gerontologist Darren Baker of the Mayo Clinic. “They were healthier until the time they died.”
Baker and colleagues’ experiment, described Nov. 2 in Nature, killed mouse cells producing a protein called p16Ink4a.
On its own, p16Ink4a — p16 for short — is just one part of the story. It’s a tumor inhibitor, but more importantly it’s what researchers call a biomarker, a sign that something else is going on. When p16 is found in a cell, that cell is probably reaching its replication limit and grinding to a senescent halt.
This slowdown, first identified in 1961 by biologists Leonard Hayflick and Paul Moorhead, is a normal part of cellular life cycles. The name for cells that divide without stopping is cancer. But research in subsequent decades, and in particular since the late 1990s, suggested that cellular senescence came with a price.