Seven studies reveal new ways to target "zombie" cells linked to ageing
US scientists have published seven studies explaining why ageing "zombie" cells cause inflammation, and early tests in older mice showed treatments, including a tomato compound, improved health.
A team of US researchers has published seven studies that shed fresh light on so-called “zombie” cells, the ageing cells that stop dividing but stay active in the body. The work suggests new ways to find these cells, calm the inflammation they cause and, in older mice at least, improve health.
Zombie cells, known formally as senescent cells, release inflammatory substances that can feed into diseases of later life. The studies were carried out at the Robert and Arlene Kogod Center on Aging and appeared in Nature journals. They go beyond confirming that these cells matter, asking instead how to tell different types apart and why they turn harmful.
One long-standing headache has been spotting the cells reliably. The research shows they vary considerably depending on where they sit in the body and what made them senescent. To help, the team built a tool called the SenMayo gene set, which uses patterns of gene activity to identify them across different tissues. It was tested on bone biopsies from older adults and has since become a widely used resource.
Other studies looked at why the inflammation never seems to stop. Several routes involve faulty mitochondria, the tiny structures that supply much of a cell’s energy. In one, genetic material leaking from mitochondria sets off immune responses, while another involves shifts in mitochondrial metabolism that alter how inflammatory genes are switched on.
That points to a rather neat possibility: treatments that switch off the harmful signals without having to destroy the cells themselves.
The team also tried several experimental approaches in older mice, including drugs designed to clear senescent cells, a natural compound found in tomatoes, and genetic techniques aimed at particular cell populations. Depending on the method, the mice showed lower inflammation and improvements in physical frailty, brain inflammation and performance on thinking tasks. A further study identified a protein, IL-23R, as a possible blood marker of biological ageing.
Why it matters
Chronic inflammation is tied to many conditions that become more common with age, so understanding exactly which cells drive it is a useful step towards treating them. The results are still preliminary, and further research is needed to show whether any of these approaches are safe and effective in people. Even so, a clearer map of the problem is the sort of groundwork that sensible therapies are built on.
