As we get older, our bodies become less resilient. That might mean we move less throughout the day and face a higher risk of multimorbidity (having multiple chronic diseases at once).
One of the reasons for this change may be that senescent cells, sometimes called “zombie” cells, start accumulating in our body over time. These cells secrete certain molecules that can “contribute to chronic inflammation and ageing-related diseases” if left to build up, a 2025 paper suggests.
A process called senolysis usually clears these “zombie cells” away, but later in life, that cleaning system becomes less efficient.
And now, a paper published in Nature Ageing has sought to find out why.
It might be down to how our cells get recycled
Zombie cells aren’t all bad. For instance, they can show up after an injury and send signals to other parts of your body that kickstart the healing process.
But issues happen when we can’t get rid of excess zombie cells, or perhaps (separate 2026 research suggests) the wrong kind of zombie cells.
After conducting experiments on mice, the researchers behind the Nature Ageing study noticed that problematic senescent cells seemed to accumulate when a cellular process called chaperone-mediated autophagy (CMA) slowed down.
CMA is a “highly selective” form of autophagy (the body’s natural cell recycling system).
When CMA slowed down, the change seemed to both affect the zombie cells themselves and the immune cells tasked with getting rid of them.
Dr Ana Maria Cuervo, a professor and co-director of the Institute for Geroscience at the Albert Einstein College of Medicine, said: “In older animals, age-related changes in both senescent cells and the immune cells responsible for removing them allow these zombie cells to accumulate and play a role in disease.
“By restoring cellular recycling, we may be able to help the body’s own defences clear these cells more effectively.”
She added: “Our research connects two major drivers of ageing – declining CMA and cellular senescence – and shows for the first time how their interaction allows senescent cells to evade clearance by the immune system in old organisms.”
When researchers restored CMA in mice, senescent cell buildup seemed to decrease across all tissues. And it appeared to lower the severity of pulmonary fibrosis – a condition linked to zombie cells – in mouse models, too.
Previous research from Dr Cuervo had also linked slower CMA to brain changes that could increase our dementia risk.
Perhaps killing zombie cells outright might not be the only answer
Other research had suggested that selectively “deleting” zombie cells might help to make us more resilient as we age.
But this study hints at alternative possible therapies.
“We’ve also found that instead of trying to kill zombie cells, we may be able to restore their interaction with the immune system so that the body can clear them naturally,” Dr Curevo explained in a press release.
“The next challenge is determining whether this approach can eventually be developed into a safe treatment for age-related diseases in people.”
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