Latest news with #senescentCells
Yahoo
6 days ago
- Health
- Yahoo
AI-Assisted Technique Can Measure and Track Aging Cells
NEW YORK, July 7, 2025 /PRNewswire/ -- A combination of high-resolution imaging and machine learning, also known as artificial intelligence (AI), can track cells damaged from injury, aging, or disease, and that no longer grow and reproduce normally, a new study shows. These senescent cells are known to play a key role in wound repair and aging-related diseases, such as cancer and heart disease, so tracking their progress, researchers say, could lead to a better understanding of how tissues gradually lose their ability to regenerate over time or how they fuel disease. The tool could also provide insight into therapies for reversing the damage. Led by NYU Langone Health Department of Orthopedic Surgery researchers, the study included training a computer system to help analyze animal cells damaged by increasing concentrations of chemicals over time to replicate human aging. Cells continuously confronted with environmental or biological stress are known to senesce, meaning they stop reproducing and start to release telltale molecules indicating that they have suffered injury. Publishing in the journal Nature Communications online July 7, the researchers' AI analysis revealed several measurable features connected to the cell's control center (nucleus), that, when taken together, closely tracked with the degree of senescence in the tissue or group of cells. This included signs that the nucleus had expanded, had denser centers or foci, and had become less circular and more irregular in shape. Its genetic material also stained lighter than normal with standard chemical dyes. Further testing confirmed that cells with these characteristics were indeed senescent, showing signs that they had stopped reproducing, had damaged DNA, and had densely packed enzyme-storing lysosomes. The cells also demonstrated a response to existing senolytic drugs. From their analysis, researchers created what they term a nuclear morphometric pipeline (NMP) that uses the nucleus's changed physical characteristics to produce a single senescent score to describe a range of cells. For example, groups of fully senescent cells could be compared to a cluster of healthy cells on a scale from minus 20 to plus 20. To validate the NMP score, the researchers then showed that it could accurately distinguish between healthy and diseased mouse cells from young to older mice, age 3 months to more than 2 years. Older cell clusters had significantly lower NMP scores than younger cell clusters. The researchers also tested the NMP tool on five kinds of cells in mice of different ages with injured muscle tissue as it underwent repair. The NMP was found to track closely with changing levels of senescent and nonsenescent mesenchymal stem cells, muscle stem cells, endothelial cells, and immune cells in young, adult, and geriatric mice. For example, use of the NMP was able to confirm that senescent muscle stem cells were absent in control mice that were not injured, but present in large numbers in injured mice immediately after muscle injury (when they help initiate repair), with gradual loss as the tissue regenerated. Final testing showed that the NMP could successfully distinguish between healthy and senescent cartilage cells, which were 10 times more prevalent in geriatric mice with osteoarthritis than in younger, healthy mice. Osteoarthritis is known to progressively worsen with age. "Our study demonstrates that specific nuclear morphometrics can serve as a reliable tool for identifying and tracking senescent cells, which we believe is key to future research and understanding of tissue regeneration, aging, and progressive disease," said study senior investigator Michael Wosczyna, PhD. Wosczyna is an assistant professor in the Department of Orthopedic Surgery at the NYU Grossman School of Medicine. Wosczyna says his team's study confirms the NMP's broad application for study of senescent cells across all ages and differing tissue types, and in a variety of diseases. He says the team plans further experiments to examine use of the NMP in human tissues, as well as combining the NMP with other biomarker tools for examining senescence and its various roles in wound repair, aging, and disease. The researchers say their ultimate goal for the NMP, for which NYU has filed a patent application, is to use it to develop treatments that prevent or reverse negative effects of senescence on human health. "Our testing platform offers a rigorous method to more easily than before study senescent cells and to test the efficacy of therapeutics, such as senolytics, in targeting these cells in different tissues and pathologies," said Wosczyna, who plans to make the NMP freely available to other researchers. "Existing methods to identify senescent cells are difficult to use, making them less reliable than the nuclear morphometric pipeline, or NMP, which relies on a more commonly used stain for the nucleus," said study co-lead investigator Sahil Mapkar, BS, Mapkar is a doctoral candidate at the NYU Tandon School of Engineering. Funding for the study was provided by National Institutes of Health grant R01AG053438 and the Department of Orthopedic Surgery at NYU Langone. Besides Wosczyna and Makpar, NYU Langone researchers involved in this study are co-lead investigators Sarah Bliss, and Edgar Perez Carbajal, and study co-investigators Sean Murray, Zhiru Li, Anna Wilson, Vikrant Piprode, Youjin Lee, Thorsten Kirsch, Katerina Petroff, and Fengyuan Liu. About NYU Langone HealthNYU Langone Health is a fully integrated health system that consistently achieves the best patient outcomes through a rigorous focus on quality that has resulted in some of the lowest mortality rates in the nation. Vizient Inc. has ranked NYU Langone No. 1 out of 115 comprehensive academic medical centers across the nation for three years in a row, and U.S. News & World Report recently placed nine of its clinical specialties among the top five in the nation. NYU Langone offers a comprehensive range of medical services with one high standard of care across seven inpatient locations, its Perlmutter Cancer Center, and more than 320 outpatient locations in the New York area and Florida. With $14.2 billion in revenue this year, the system also includes two tuition-free medical schools, in Manhattan and on Long Island, and a vast research enterprise. Media ContactDavid STUDY LINKhttps:// STUDY DOI10.1038/s41467-025-60975-z View original content to download multimedia: SOURCE NYU Langone Health System
Associated Press
6 days ago
- Health
- Associated Press
AI-Assisted Technique Can Measure and Track Aging Cells
NEW YORK, July 7, 2025 /PRNewswire/ -- A combination of high-resolution imaging and machine learning, also known as artificial intelligence (AI), can track cells damaged from injury, aging, or disease, and that no longer grow and reproduce normally, a new study shows. These senescent cells are known to play a key role in wound repair and aging-related diseases, such as cancer and heart disease, so tracking their progress, researchers say, could lead to a better understanding of how tissues gradually lose their ability to regenerate over time or how they fuel disease. The tool could also provide insight into therapies for reversing the damage. Led by NYU Langone Health Department of Orthopedic Surgery researchers, the study included training a computer system to help analyze animal cells damaged by increasing concentrations of chemicals over time to replicate human aging. Cells continuously confronted with environmental or biological stress are known to senesce, meaning they stop reproducing and start to release telltale molecules indicating that they have suffered injury. Publishing in the journal Nature Communications online July 7, the researchers' AI analysis revealed several measurable features connected to the cell's control center (nucleus), that, when taken together, closely tracked with the degree of senescence in the tissue or group of cells. This included signs that the nucleus had expanded, had denser centers or foci, and had become less circular and more irregular in shape. Its genetic material also stained lighter than normal with standard chemical dyes. Further testing confirmed that cells with these characteristics were indeed senescent, showing signs that they had stopped reproducing, had damaged DNA, and had densely packed enzyme-storing lysosomes. The cells also demonstrated a response to existing senolytic drugs. From their analysis, researchers created what they term a nuclear morphometric pipeline (NMP) that uses the nucleus's changed physical characteristics to produce a single senescent score to describe a range of cells. For example, groups of fully senescent cells could be compared to a cluster of healthy cells on a scale from minus 20 to plus 20. To validate the NMP score, the researchers then showed that it could accurately distinguish between healthy and diseased mouse cells from young to older mice, age 3 months to more than 2 years. Older cell clusters had significantly lower NMP scores than younger cell clusters. The researchers also tested the NMP tool on five kinds of cells in mice of different ages with injured muscle tissue as it underwent repair. The NMP was found to track closely with changing levels of senescent and nonsenescent mesenchymal stem cells, muscle stem cells, endothelial cells, and immune cells in young, adult, and geriatric mice. For example, use of the NMP was able to confirm that senescent muscle stem cells were absent in control mice that were not injured, but present in large numbers in injured mice immediately after muscle injury (when they help initiate repair), with gradual loss as the tissue regenerated. Final testing showed that the NMP could successfully distinguish between healthy and senescent cartilage cells, which were 10 times more prevalent in geriatric mice with osteoarthritis than in younger, healthy mice. Osteoarthritis is known to progressively worsen with age. 'Our study demonstrates that specific nuclear morphometrics can serve as a reliable tool for identifying and tracking senescent cells, which we believe is key to future research and understanding of tissue regeneration, aging, and progressive disease,' said study senior investigator Michael Wosczyna, PhD. Wosczyna is an assistant professor in the Department of Orthopedic Surgery at the NYU Grossman School of Medicine. Wosczyna says his team's study confirms the NMP's broad application for study of senescent cells across all ages and differing tissue types, and in a variety of diseases. He says the team plans further experiments to examine use of the NMP in human tissues, as well as combining the NMP with other biomarker tools for examining senescence and its various roles in wound repair, aging, and disease. The researchers say their ultimate goal for the NMP, for which NYU has filed a patent application, is to use it to develop treatments that prevent or reverse negative effects of senescence on human health. 'Our testing platform offers a rigorous method to more easily than before study senescent cells and to test the efficacy of therapeutics, such as senolytics, in targeting these cells in different tissues and pathologies,' said Wosczyna, who plans to make the NMP freely available to other researchers. 'Existing methods to identify senescent cells are difficult to use, making them less reliable than the nuclear morphometric pipeline, or NMP, which relies on a more commonly used stain for the nucleus,' said study co-lead investigator Sahil Mapkar, BS, Mapkar is a doctoral candidate at the NYU Tandon School of Engineering. Funding for the study was provided by National Institutes of Health grant R01AG053438 and the Department of Orthopedic Surgery at NYU Langone. Besides Wosczyna and Makpar, NYU Langone researchers involved in this study are co-lead investigators Sarah Bliss, and Edgar Perez Carbajal, and study co-investigators Sean Murray, Zhiru Li, Anna Wilson, Vikrant Piprode, Youjin Lee, Thorsten Kirsch, Katerina Petroff, and Fengyuan Liu. About NYU Langone Health NYU Langone Health is a fully integrated health system that consistently achieves the best patient outcomes through a rigorous focus on quality that has resulted in some of the lowest mortality rates in the nation. Vizient Inc. has ranked NYU Langone No. 1 out of 115 comprehensive academic medical centers across the nation for three years in a row, and U.S. News & World Report recently placed nine of its clinical specialties among the top five in the nation. NYU Langone offers a comprehensive range of medical services with one high standard of care across seven inpatient locations, its Perlmutter Cancer Center, and more than 320 outpatient locations in the New York area and Florida. With $14.2 billion in revenue this year, the system also includes two tuition-free medical schools, in Manhattan and on Long Island, and a vast research enterprise. Media Contact David March 212-404-3528 [email protected] STUDY LINK STUDY DOI 10.1038/s41467-025-60975-z View original content to download multimedia: SOURCE NYU Langone Health System
Telegraph
08-05-2025
- Health
- Telegraph
Why the key to slowing down ageing is targeting ‘zombie' cells
At last year's British Society for Research on Ageing conference, an annual meeting to discuss the latest ideas for improving healthy ageing and lifespan, one theme kept cropping up – how best to rid the body of senescent cells? Often dubbed 'zombie cells,' because instead of replicating and then dying off like most healthy cells in our body, senescent cells stop dividing and instead simply linger, refusing to disappear. They were first discovered in the 1960s but have attracted growing attention in the past two decades, because their steady accumulation throughout our lives is increasingly being implicated in almost all age-related diseases and even the underlying ageing process itself. 'They've been described as the undead cells, and they seem to be a common denominator in almost every single major age associated disease that has been ever looked at,' says Dr Johannes Grillari, the director of the Ludwig Boltzmann Institute for Traumatology in Vienna, who studies senescent cells. 'You see this whether it's cardiovascular diseases, neurodegenerative diseases, musculoskeletal diseases, lung fibrosis, chronic kidney disease. Name any one of these killers, and senescent cells are there.' The flip side of this, of course, is that by removing them, we might actually have a new means of curing many diseases, and perhaps even slowing the underlying ageing process. Because of this, research into senolytics – drugs capable of removing senescent cells – is now one of the active areas of longevity science, with dozens of clinical trials underway around the world. So what causes these zombie cells to form, can we stop them, and what do we know about future drugs? What are senescent cells? At the Mayo Clinic in Rochester, Minnesota, the geriatrician and medical professor James Kirkland is one of the world's leading experts on senescent cells. He explains that while excessive numbers can harm us, our body has evolved to harbour these cells for a number of reasons – they're involved in everything from childbirth to wound healing. 'It's actually molecules produced by senescent cells that appear to drive the baby through the birth canal in the last five days of pregnancy,' he says. Likewise, the formation of these zombie cells also acts as one of the body's inbuilt protective mechanisms against cancer development. Over our lifetimes, this prevents numerous individual cancer cells from continuing to grow and form a tumour. 'Senescence means that cells carrying cancerous mutations in their DNA then stop dividing, preventing them from developing into a rapidly growing cancer,' says Prof Kirkland. However, the problem is that as we age, we gradually accumulate more and more senescent cells. While they no longer divide, they are still metabolically active, which means they're still able to communicate with surrounding cells by producing continuous streams of molecules. In particular, some zombie cells start to generate large quantities of pro-inflammatory cytokines – proteins which are associated with chronic inflammation. 'By the time we reach old age, we have senescent cells in many of our tissues, creating this chronic low-grade inflammation,' says Dr Grillari. 'We think that's their most detrimental activity.' How they affect the body While we can accumulate zombie cells in every single one of our organs, there are some where they have been particularly implicated in disease. Spine and joints Zombie cells building up in spinal discs – cushion-like structures that sit between the vertebrae – either as a result of ageing or damage, have been associated with back pain. The same is true for the knees and ankles where growing numbers of zombie cells in the cartilage and soft tissues which line the inner surface of our joints, cause inflammation and loss of flexibility. This has been linked to osteoarthritis, the degenerative joint disease which represents the most common form of arthritis. Liver, pancreas, gut and fat tissue At Amsterdam University Medical Centre, the gastroenterologist Dr Stijn Meijnikman has been studying the role of zombie cells in common metabolic diseases, from Type 2 diabetes to non-alcoholic fatty liver disease. According to Dr Meijnikman, the development of these diseases is linked to zombie cells accumulating in many of the internal organs, as well as the gut and even fat tissue. Because these cells are no longer working as they should, this leads to loss of organ function and the formation of scar tissue. 'In all metabolic diseases, we can see these senescent cells popping up everywhere,' he says. Kidneys Studies have previously linked zombie cells to kidney and other organ transplant failures, one of the reasons why organs donated by people over the age of 60 make for less successful transplant candidates. 'There's been papers that have shown that the more senescent cells you have in a transplant organ, the worse the outcome of the transplantation,' says Dr Grillari. Eyes Our ability to see owes much to lens epithelial cells, those which are responsible for the growth and development of the eye lens. However, with age or damage – for example from excessive exposure to UV light, as a result of not wearing sunglasses - these cells can become senescent, leading to the eventual formation of cataracts. Brain In 2022, a study from American researchers backed by the US National Institute on Ageing found that patients with Alzheimer's disease have considerably more zombie cells in their brains than those who are cognitively normal. The research suggested senescence could contribute to the build-up of toxic tau tangles in the brain which represent one of the hallmarks of the disease. Senescent cells and ageing So what makes us more vulnerable to accumulating senescent cells, and is there anything we can do to protect ourselves? Three years ago, a study from the Mayo Clinic indicated that physical inactivity is a major cause of prematurely accumulating large numbers of zombie cells, while on the other hand, regular moderate-vigorous activity may help by kicking the immune system into gear and provoking it to clear these cells. One study of 170 healthy participants aged between 18 and 80 found that doing more than 240 minutes a month of any form of moderate physical activity (for example running, swimming, and cycling) leads to fewer zombie cells. Resistance training using weights or press-ups may also help, with one study of overweight and obese women in their 70s, finding that five months of resistance training resulted in fewer zombie cells in their fat tissue. At the same time, the relationship between exercise and senescence is not straightforward. Some studies have indicated that forms of exercise where the body is pushed to extreme exhaustion, for example ultra-marathon running or attempting endurance challenges without sufficient training, could push you to accumulate more of these cells. Last year, another study suggested that adequate levels of sleep, intermittent fasting, consuming enough dietary fibre and commonly available probiotics, such as Lactobacillus, may help reduce your levels of zombie cells. On the other hand, regularly consuming excess alcohol, smoking, exposure to sunlight without sufficient protection and chronic stress drives the formation of these cells. Can you get rid of senescent cells? But for people who have already accumulated large numbers of zombie cells which are contributing to different diseases, the main hope is future drug treatments which can rid these cells from the body, an emerging class of medicines known as senolytics. Over the last decade, Prof Kirkland has pioneered studies on a series of compounds, which include the chemotherapy drug dasatinib and high doses of two natural plant chemicals quercetin and fisetin, originally found in various fruits and vegetables. His work, and that of others, has shown that they can help eliminate zombie cells by disabling the biological pathways which allow them to persist, causing them to self-destruct. Dr Katarzyna Whysall, an associate professor at the University of Galway, describes these three senolytics as already showing great promise in tackling various age-related disorders. One human trial, carried out by Prof Kirkland in patients with a form of chronic lung disease, found that three weeks of treatment with dasatinib and quercetin improved their physical strength in various ways. 'Another small study found encouraging results for senolytics use in Alzheimer's disease, although more research is still needed,' she says. Other senolytics are also currently being researched. A recently published study from Canadian scientists found that two drug candidates, called o-vanillin and RG-7112, demonstrated the ability to clear zombie cells from spinal discs in mice, suggesting that they could potentially represent a future treatment for back pain. But at the moment, the most well-characterised senolytics are dasatinib and quercetin and this treatment combination is currently being investigated in several more human trials ranging from early Alzheimer's disease to chronic kidney disease. Dr Meijnikman is currently leading a Dutch government-funded trial investigating the potential of these drugs to reverse non-alcoholic fatty liver disease. 'Based on studies in mice, if you can clear the senescent cells from the liver, you get rid of the fibrosis [a medical term for scarring],' says Dr Meijnikman. 'Of course, humans are different which is why we're doing this proof-of-concept trial for 21 weeks with a liver biopsy before and after. If we can see a decrease in fibrosis in this very short-term trial, that would create an incentive for longer trials with more patients.' At the same time, Dr Meijnikman is keen to emphasise that people should not try taking these drugs at home, and we're still far from a point where they can be given to healthy mid-lifers to see if they can help slow ageing. For example, one very real risk of clearing too many zombie cells with senolytics drugs which needs to be assessed in these trials is that this could make people more vulnerable to developing cancers. 'This is why at the moment they're only being given in clinical settings to people who already have severe disease, who could benefit from them,' he says. 'With our trial, we're trying to do a 'hit and run' approach where just for a few weeks, we temporarily disrupt these pathways which are allowing senescent cells to survive, enough to clear them but hopefully without risking longer term side effects.'
