Mayo Clinic says seven of its studies shed new light on senescent cells. These are often called “zombie” cells because they stop dividing but stay active in the body, releasing inflammatory substances linked to diseases of older age1. The studies look at how to recognize different kinds of these cells, why they keep producing harmful inflammation, and how that might be reduced1. When experimental treatments were tried in older mice, Mayo reported less inflammation and better physical and brain health, depending on the approach1. None of the new treatment results come from people.
What happened
The research was published in Nature journals and carried out at Mayo Clinic’s Robert and Arlene Kogod Center on Aging, according to a Mayo release dated October 26, 20261. Mayo describes the work as going beyond confirming that zombie cells matter in aging. It focuses on telling them apart and finding new ways to blunt their effects1.
“This body of work is moving the aging field forward to precisely identify, understand and target the specific senescent cells that contribute to age-related dysfunction,” said Marissa Schafer, a Mayo Clinic scientist whose lab directed several of the studies1.
What the studies found
Zombie cells are not all alike
A long-standing problem in the field is spotting these cells reliably. The new work reports that they vary more than once thought. Their features differ by where they sit in the body and by what pushed them into the zombie state1. To deal with this, the team built a tool called the SenMayo gene set. It reads patterns of gene activity to flag senescent cells more consistently across tissues1. The researchers tested it on bone samples taken from older adults. They also found that the gene pattern faded after zombie cells were removed in animal and lab experiments1. Mayo says SenMayo is already widely used by other researchers. Endocrinologist Sundeep Khosla was senior author of that paper1.
The cell’s power plants keep the fire going
Other studies asked why zombie cells keep sending out inflammatory signals. Several of the answers involve faulty mitochondria, the tiny structures that make much of a cell’s energy1. In one pathway, DNA and RNA from mitochondria set off immune responses that drive inflammation. In another, changes in how mitochondria handle fuel alter which inflammation genes are switched on, without changing the DNA itself1. João Passos was senior author of three papers on these mechanisms and on the variety of zombie cells. One title states that leaking mitochondrial RNA “drives” the cells’ inflammatory output1.
This builds on an earlier Passos study in Nature. There, the team saw a small group of “rogue” mitochondria in zombie cells start a self-destruct process and release their DNA into the cell’s interior. The cell treats this DNA as foreign, which sparks inflammation2. Blocking that process in mice equal in age to a 70-year-old person reduced tissue inflammation and improved strength, balance and bone structure, according to Mayo2.
Mayo says these findings suggest it may one day be possible to calm the inflammation while leaving the zombie cells in place. That would be a different strategy from trying to destroy every one of them1.
Treatments tested in older mice
The team also tried to reduce the number of zombie cells or limit the harm they do. The approaches included senolytic drugs, which are designed to kill senescent cells, a natural compound found in tomatoes, and genetic methods aimed at specific groups of aging cells1. In older mice, depending on the approach, the researchers saw lower inflammation markers and improvements in physical frailty, inflammation in the brain and performance on thinking tasks1.
A possible blood measure
Another study pointed to a possible way of measuring parts of biological aging with a blood test. It involves a molecule called IL-23R1. The release text available to Biohack breaks off at this point, so details of that finding are not reported here.
What it does not show yet
The treatment results described in the release come from mice1. Mouse studies can show how a process works and whether an approach is worth testing. They cannot show that it is safe or helpful for people. The release does not give the number of animals, the size of the effects, the doses used, or the name of the tomato compound. It also does not give publication dates for each of the seven papers1. Mayo itself frames the work as “groundwork” for future therapies, not as a treatment ready for use1.
Earlier human results on zombie-cell drugs have been mixed. In a 2024 Mayo trial, 60 healthy women past menopause took dasatinib, a cancer drug, plus quercetin, a natural compound found in some foods, on and off for 20 weeks. The pair helped bone formation but did not reduce bone breakdown. It mainly benefited women with signs of many zombie cells3. Khosla said at the time that the findings “argue against what many people are already doing,” taking products like quercetin or fisetin without knowing whether they would benefit or what dosing would be safe3.
Who is behind it
The work feeds into the Cellular Senescence Network (SenNet) Consortium. This is a US effort to map where zombie cells occur in the human body and how they change over a lifetime, funded by the National Institutes of Health Common Fund1. The release does not list conflicts of interest for the seven papers.
Earlier Mayo work in this area has involved financial ties. In the 2024 bone trial, Mayo researchers Nathan LeBrasseur, Tamara Tchkonia and James Kirkland had financial interests related to the research, including Mayo Clinic patents and pending patents on senolytic drugs3. LeBrasseur is also listed as a contributor to the new SenMayo paper1. In 2017, Mayo Clinic and several researchers, including Kirkland and Tchkonia, disclosed a financial interest in a study of new senolytic drugs4.
How it fits the field
Mayo has long been at the center of this research. Kirkland, then director of the Kogod Center, said in 2017 that Mayo “discovered the first senolytic drugs,” which eased a range of age-related problems in mice4. That year his team reported that fisetin and two other compounds cleared zombie cells in human cells grown in a dish5. The best-known approach, dasatinib plus quercetin, was identified in 2015 by the Kirkland lab. It is usually given for two days in a row every few weeks6.
Human testing continues. A Mayo-sponsored early trial called ALSENLITE gives dasatinib and quercetin to people with mild memory problems or Alzheimer’s disease. Participants take the drugs two days out of every 15, for six cycles, with no placebo group7. An industry overview from May 2026 described the first decade of human trials of these drugs as “messy.” It pointed to a small Dutch early trial of a newer compound as the first clear signal in patients6.
The new studies push in two directions. One is better tools to tell zombie cells apart, since they appear to differ by tissue1. The other is ways to shut off their inflammation without killing them1. Both respond to a lesson from the 2024 trial: these drugs are not “one-size-fits-all”3.
What to watch next
- Whether the full papers report effect sizes and safety findings for the mouse treatments, including the tomato compound1.
- Whether approaches that block the inflammation without killing zombie cells move toward testing in people1.
- Further details on the IL-23R blood measure1.
- Results from human trials of zombie-cell drugs, such as the ALSENLITE study in Alzheimer’s disease7.
- New maps of zombie cells across the body from the SenNet Consortium1.
