This protective enzyme could help stop fatty liver disease from getting worse

 

A newly identified protective enzyme could offer scientists a new way to stop fatty liver disease before it causes serious liver damage. Credit: Shutterstock

Researchers co-led by Cedars-Sinai Health Sciences University have identified an enzyme that may help protect the liver from the damage that can occur as the most common form of liver disease becomes more severe. The findings, from a preclinical study published in Nature Metabolism, could eventually support new strategies for preventing serious liver injury and progression toward liver failure.

An estimated 100 million people in the U.S. have metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called nonalcoholic fatty liver disease, according to the American Liver Foundation. Roughly 20% to 25% of those affected go on to develop metabolic dysfunction-associated steatohepatitis (MASH), a more serious form of the condition in which excess liver fat is accompanied by inflammation, cell injury and scarring.

Why MASH Is Difficult to Treat

Current care mainly centers on lifestyle changes and efforts to limit additional liver damage. Although medications are available, treatment options are still limited, and there is currently no cure for MASH.

Earlier research has suggested that damaged mitochondria, the structures that produce energy for cells, may contribute to the development and progression of MASH. In the new multicenter study, Cedars-Sinai researchers found that levels of an enzyme called UBE2N decline in liver cells as the disease becomes more advanced.

"The UBE2N enzyme appears to protect the liver from the inflammation and damage associated with MASH by helping remove damaged mitochondria and supporting the breakdown of fat," said Ekihiro Seki, MD, PhD, professor of Medicine and Biomedical Sciences at Cedars-Sinai and co-corresponding author of the study. "When levels of the enzyme fell, we saw more damaged cells and injury to the liver."

Restoring UBE2N Reduced Liver Damage in Mice

The researchers then restored UBE2N to normal levels in the livers of laboratory mice. After doing so, they observed reductions in fat accumulation, inflammation and scarring.

Those results suggest that UBE2N could become a potential treatment target for preventing MASLD from advancing to MASH.

"The identification of this enzyme's role in regulating mitochondria in the liver is an important advance in understanding steatotic liver disease," said Shelly Lu, MD, the Women's Guild Chair in Gastroenterology and director of the Karsh Division of Gastroenterology and Hepatology at Cedars-Sinai. "Future studies can test whether enhancing this protective pathway can complement existing treatments, identify patients most likely to benefit and lead to new therapeutic approaches for preventing advanced disease."

Additional Cedars-Sinai authors include Michitaka Matsuda, So Yeon Kim, Takashi Tsuchiya and Yoon Seok Roh.

Additional authors include: Feng Wang, Jin Lee, Jeong-Su Park, Meizhou Huang, Hwan Ma, Guoyan Sui, Zixiong Zhou, Xufeng Wu, Haram Lee, Soohwan Oh, Hanseul Park, Key-Hwan Lim, Chun-Woong Park, Sang-Bae Han, Jin Tae Hong and Michael Karin.

Funding: This work was supported by the National Research Foundation of Korea (grant nos. RS-2025-02273102 and RS-2025-02603096), Regional Innovation System & Education (RISE) programme of Chungbuk (grant no. 2025-RISE-11-014-03), the Pinnacle Research Award of American Association for the Study of Liver Diseases (AASLD, to J.L.), the San Diego Digestive Diseases Research Center (SDDRC) Pilot/Feasibility Grant (NIDDK P30 DK120515, to J.L.), the National Institutes of Health (grant nos. R01DK085252, R01DK138591 and R01CA301632) and the National Natural Science Foundation of China (grant no. 82404726).

Journal Reference:

1. Feng Wang, Jin Lee, Jeong-Su Park, Meizhou Huang, Hwan Ma, Guoyan Sui, Zixiong Zhou, Michitaka Matsuda, So Yeon Kim, Takashi Tsuchiya, Xuefeng Wu, Haram Lee, Soohwan Oh, Hanseul Park, Key-Hwan Lim, Chun-Woong Park, Sang-Bae Han, Jin Tae Hong, Michael Karin, Yoon Seok Roh, Ekihiro Seki. UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis. Nature Metabolism, 2026; 8 (9): 1926 DOI: 10.1038/s42255-026-01590-0

Courtesy:

Cedars-Sinai. "This protective enzyme could help stop fatty liver disease from getting worse." ScienceDaily. ScienceDaily, 3 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261002080020.htm>.

 

 

Your gut may be making a molecule that raises Alzheimer’s risk

 

A compound made by gut bacteria may quietly raise Alzheimer’s risk and speed cognitive decline, giving scientists a promising new treatment target. Credit: Shutterstock

A molecule made by bacteria in the digestive system may increase the risk of Alzheimer's disease and accelerate cognitive decline in people with dementia, according to new research. The finding could point scientists toward a potential treatment strategy aimed at lowering Alzheimer's risk.

Nearly a decade ago, a research team led by University of Wisconsin-Madison professors Barbara Bendlin and Federico Rey found that the mix of microorganisms living in the intestines differs between people with Alzheimer's disease and healthy individuals.

"Since then, we've been trying to figure out how this difference in the gut perhaps leads to changes in the brain," says Bendlin, a professor of medicine in the UW School of Medicine and Public Health.

A Gut Molecule With Effects Beyond the Intestines

In a recent study published in the journal Nature Communications, Bendlin, Rey and their collaborators focused on imidazole propionate (ImP), a compound produced by certain bacteria in the gut. Their findings suggest that ImP may contribute to brain changes involved in Alzheimer's disease and related forms of dementia.

ImP production varies considerably from person to person. Some people appear to generate relatively large amounts, while others produce very little.

"ImP-producing bacteria are present in a large fraction of people, but they're not very abundant in most people," says Rey, a UW-Madison professor of bacteriology. "But something we have learned over the years is that a microbe doesn't have to be abundant to have an impact on the host."

Once produced in the gut, ImP can enter the circulation and reach other parts of the body. Previous research has linked the compound to type 2 diabetes and coronary artery disease.

The new study suggests that its effects may also extend to the brain. In mice, researchers found that ImP reaching the brain increased the accumulation of abnormal beta amyloid and tau proteins, two major hallmarks associated with Alzheimer's disease.

"That process eventually results in the death of neurons, and in humans is a key feature of Alzheimer's disease," Rey says.

Higher ImP Levels Linked to Faster Cognitive Decline

The researchers then examined blood samples from almost 1,200 people enrolled in the Wisconsin Registry for Alzheimer's Prevention and studies conducted through the Wisconsin Alzheimer's Disease Research Center.

Participants with higher concentrations of ImP in their blood were much more likely to show biological markers associated with abnormal proteins and impaired neuron function in dementia.

Because the volunteers had also completed cognitive testing over time, the researchers were able to compare ImP levels with changes in thinking and memory.

"And because we have the results of cognitive tests these volunteers took over time, we can see that the people with the highest ImP levels also experienced much faster cognitive decline," Rey says.

The team also discovered a genetic variation associated with substantially higher levels of ImP in the bloodstream. About 43% of the people in the study carried this variation.

Researchers suspect the genetic difference may influence how effectively the kidneys remove ImP from the blood, affecting how much of the compound remains in circulation.

"This genetic variation has been associated with increased Alzheimer's risk in large genetic studies before, and now we may understand why it's connected," Rey says.

A Potential New Target for Alzheimer's Prevention

One of the most important possibilities raised by the findings is that ImP itself could become a target for preventing or slowing Alzheimer's disease and related dementias.

However, reducing ImP through diet alone may not be straightforward. Gut bacteria produce the compound while generating energy from histidine, an amino acid that is essential for human health and found in many foods, particularly foods rich in protein.

"Generally improving your diet would probably help," Bendlin says. "But it's not as easy as saying, 'Stop eating eggs' or 'Don't eat so much red meat.' Because you need histidine, and it's all over the place."

Rather than trying to eliminate histidine from the diet, the researchers say the discovery could eventually lead to treatments that specifically reduce ImP levels in the bloodstream.

Identifying a particular molecule and a related genetic variation gives scientists a more precise target to investigate.

"It could be just like cholesterol, where people with elevated cholesterol take a drug, a statin, that reduces their risk for heart disease," Bendlin says. "If we can find an inhibitor that can help decrease the levels of ImP in the blood, that could hopefully reduce the risk of Alzheimer's and the speed of cognitive decline for a significant number of people."

Scientists from the University of California, Los Angeles and the University of Gothenburg also contributed to the study.

This research was supported in part by grants from the Wisconsin Partnership Program and the National Institutes of Health (R01AG070973, R01AG083883, R01AG092220, R21AG089348, R01HL168493, R01DK143650 and U54HL170326) and the U.S. Department of Agriculture (WIS03073).

Journal Reference:

1. Vaibhav Vemuganti, Jea Woo Kang, Qijun Zhang, Eric R. McGregor, James R. Hilser, Ruben Aquino-Martinez, Sandra Harding, Joseph Lawrence Harpt, Katharina R. Beck, Hailey Bussan, Jessamine F. Kuehn, Yuetiva Deming, Rachel Studer, Sterling C. Johnson, Sanjay Asthana, Henrik Zetterberg, Kaj Blennow, Corinne D. Engelman, Hooman Allayee, Rozalyn M. Anderson, Tyler K. Ulland, Fredrik Bäckhed, Barbara B. Bendlin, Federico E. Rey. Gut bacterial metabolite imidazole propionate potentiates Alzheimer’s disease pathology. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-74744-z

Courtesy:

University of Wisconsin-Madison. "Your gut may be making a molecule that raises Alzheimer’s risk." ScienceDaily. ScienceDaily, 3 October 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260930225459.htm>. 

 

Your gut bacteria may offer an early clue to how quickly your brain is aging

 

A UCLA study suggests that signs of faster brain aging may be connected to the bacteria and chemical compounds living in the gut, even in generally healthy adults. Credit: Shutterstock

A new UCLA study suggests that the pace of brain aging may be connected to bacteria in the gut and the chemical compounds they produce. The findings offer a new look at biological changes that may begin long before noticeable problems with memory or thinking appear.

Scientists have used brain scans for years to estimate a person's "brain age," which can differ from chronological age. Previous research has found that when the brain appears older than expected, that pattern can be associated with poorer memory, weaker thinking skills and changes in mood.

Most earlier studies, however, focused on older adults or people who already had neurological conditions. That left an important question unanswered: does an older looking brain also matter in younger, generally healthy adults?

Measuring How Old the Brain Appears

In a new study published in the journal eBioMedicine, UCLA Health researchers examined brain scans from nearly 1,500 adults divided across three separate groups.

The team used a scanning approach that measures how different areas of the brain communicate with one another while a person is at rest. Researchers then created a computer model that estimated each person's age based on those communication patterns.

They compared the estimated brain age with each participant's actual age. The difference between the two became what the researchers called the Brain Aging Index (BAI).

Older-Looking Brains Were Linked to Memory and Mood

Across all three groups, participants whose brains appeared older than their chronological age generally performed worse on tests of working memory and executive function. Those abilities help people hold information in mind, stay focused, plan, and organize.

People with a higher Brain Aging Index also reported more symptoms of depression. The patterns repeatedly involved brain regions associated with memory and self-referential thought, or the mental processes people use when thinking about themselves and their own experiences.

Gut Bacteria Offer Another Clue

For one of the study groups, the researchers also examined stool samples to see whether differences in brain aging were connected to changes in the gut.

They found that a higher Brain Aging Index was associated with specific gut bacteria and several metabolic byproducts. These included certain fat molecules, a cholesterol-related compound and lower levels of a hormone called estetrol.

The pathways connected with these biological signals involved the immune system, blood vessel function, communication between brain cells and the processes cells use to produce energy.

Signs of Brain Aging May Appear Decades Early

"Brain aging doesn't suddenly begin when we get older, but the biological signals may be detectable decades earlier," said the study's senior author Dr. Arpana Church, co-director of the Goodman-Luskin Microbiome Center at UCLA Health. "By linking these early brain changes with the gut microbiome and its metabolites, we are beginning to identify pathways that could ultimately help us understand who may be at risk and, importantly, where we might intervene to support healthier brain aging. This ultimately opens the door to exploring whether targeting gut health could one day support healthier brain aging."

Church said the findings may eventually help researchers identify people at greater risk of cognitive or mood-related decline earlier in life. They also raise the possibility that the gut could become a target for future strategies designed to support brain health and prevention earlier in life.

Journal Reference:

1. Kanhao Zhao, Gabriel A. Vignolle, Jennifer S. Labus, Emeran A. Mayer, Allison Vaughan, Marika Dy, Priten Vora, Ming W. Hung, Keith Vossel, Chris Gill, Daniele Del Rio, Catherine Stanton, R. Paul Ross, John F. Cryan, Rima Kaddurah-Daouk, Yu Zhang, Arpana Church. Brain-gut crosstalk associated with brain ageing in young and mid-life adults: a multicohort cross-sectional study. eBioMedicine, 2026; 132: 106468 DOI: 10.1016/j.ebiom.2026.106468

Courtesy:
University of California - Los Angeles Health Sciences. "Your gut bacteria may reveal how fast your brain is aging." ScienceDaily. ScienceDaily, 4 October 2026. <www.sciencedaily.com / releases / 2026 / 10 / 261001214106.htm>. 

 

One CRISPR treatment cut “bad” cholesterol in half for a full year

 

A single CRISPR infusion cut “bad” cholesterol and triglycerides by about half for a full year in an early human trial. Credit: Shutterstock

A first-in-human Phase 1 clinical trial from Cleveland Clinic found that a single infusion of a CRISPR-Cas9 gene-editing therapy produced lasting reductions in LDL ("bad") cholesterol and triglycerides in people with lipid disorders that had not responded adequately to medications.

The study followed 15 patients for one year to determine whether the cholesterol and triglyceride reductions previously reported after two months would continue over time. After 12 months, participants who received the highest dose had a 52.5% reduction from baseline in LDL cholesterol and a 47.8% drop in triglycerides.

No serious adverse events related to the therapy were reported during the one-year follow-up.

Cholesterol Reductions Lasted for a Year

The findings were presented at the 2026 European Society of Cardiology annual meeting and published at the same time in the New England Journal of Medicine.

"Building upon the initial data presented in November 2025, the durability of the lipid-lowering effect was impressive," said Cleveland Clinic cardiologist Luke Laffin, M.D., first author of the study."It is encouraging that there were no serious safety events related to CTX310 in the trial and in the year following treatment. We look forward to continuing to investigate this therapy in a larger number of patients."

CRISPR-Cas9 is a gene-editing technology designed to make targeted changes to specific parts of a person's DNA. Researchers are studying it as a potential way to treat serious diseases by altering genes that contribute to those conditions.

How CTX310 Targets Blood Fats

The experimental treatment tested in the trial, called CTX310, is given as a one-time infusion. It carries the CRISPR editing system to the liver, where it switches off a gene known as ANGPTL3.

ANGPTL3 helps regulate fats circulating in the blood. Disabling the gene can reduce LDL cholesterol and triglycerides, both of which are associated with cardiovascular disease.

During the study, patients received CTX310 at doses ranging from 0.1 to 0.8 mg/kg. Before the infusion, they were treated with corticosteroids and antihistamines.

Researchers then monitored participants for treatment safety and measured changes in ANGPTL3, LDL cholesterol, and triglyceride levels.

At the highest dose, CTX310 lowered both LDL cholesterol and triglycerides by about 50% on average 12 months after treatment.

Long-Term Monitoring Will Continue

Although the early results are encouraging, CTX310 remains experimental and the study involved only 15 people.

Participants were monitored for one year after treatment, and researchers plan to continue long-term safety follow-up for another 15 years, in line with FDA recommendations for gene-editing therapies.

The study was funded by CRISPR Therapeutics AG; Zug, Switzerland.

Dr. Laffin's institution has received research funding from Crispr Therapeutics.

Journal Reference:

1. Luke J. Laffin, Stephen J. Nicholls, Russell S. Scott, Peter M. Clifton, Renate Koops, Ashish Sarraju, Shweta Singh, Qiuqing Wang, Kathy Wolski, Huansheng Xu, Jen Nielsen, Naimish Patel, Jason M. Duran, Steven E. Nissen. Durability of CRISPR-Cas9 Gene Editing Targeting ANGPTL3 with CTX310. New England Journal of Medicine, 2026; DOI: 10.1056/NEJMc2609825

Courtesy:

Cleveland Clinic. "One CRISPR treatment cut “bad” cholesterol in half for a full year." ScienceDaily. ScienceDaily, 27 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260925005434.htm>. 

 

Glucosamine, a popular joint supplement, linked to faster Alzheimer’s progression

 

A widely used supplement for joint pain has been linked to a potentially concerning outcome in people with early cognitive problems.

Researchers at the University of Florida found that glucosamine use was associated with a greater likelihood that mild cognitive impairment would progress to dementia. Mild cognitive impairment, often shortened to MCI, describes measurable problems with memory or thinking that are greater than expected with normal aging but do not necessarily interfere substantially with everyday life.

The findings come from a large retrospective analysis of patient health records, supported by experiments involving human brain tissue and mouse models of Alzheimer's disease. The results remain preliminary and will need to be tested in a human clinical trial, but the researchers say they add to growing evidence that disrupted metabolism may play an important role in neurodegeneration.

The study was published in Nature Metabolism.

A Popular Supplement Comes Under Scrutiny

"In the United States, there are about 7 million people living with Alzheimer's and millions more with related dementias such as Lewy body or frontotemporal dementia," said senior author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation of UF's McKnight Brain Institute. "A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse."

Glucosamine is widely sold without a prescription and is especially popular among older adults who take it for joint discomfort and joint health. Because of how commonly it is used, the researchers wanted to know whether it might influence Alzheimer's disease and related dementias, known as ADRD.

Working with Yi Guo, Ph.D., and Jiang Bian, Ph.D., the team used artificial intelligence to analyze deidentified UF Health records collected from 2012 to 2024.

The researchers focused on patients diagnosed with either ADRD or mild cognitive impairment, or MCI. In both groups, 8% of patients reported using glucosamine. That included 1,896 people with ADRD and 2,750 people with MCI.

Glucosamine Linked to Dementia Progression

After accounting for age, sex and demographics, the researchers found that glucosamine use was associated with a 25% higher likelihood that mild cognitive impairment would progress to dementia.

Among people who already had ADRD, glucosamine use was also associated with a 25% higher mortality risk, meaning a greater likelihood of death during a defined period of time.

The researchers did not observe that mortality association in the MCI group. That difference suggests glucosamine may have a stronger effect once dementia is already established.

Importantly, the health record findings do not show that glucosamine itself causes dementia to progress. Observational studies can reveal associations, but other differences between people who take a supplement and those who do not may contribute to the results.

"The electronic health record data are very provocative," said Matt Gentry, Ph.D., chair of UF's Department of Biochemistry and Molecular Biology and a study co-author. "While it's an association and not proof of causality, it does raise an important clinical question that now deserves much more attention."

A Metabolic Pathway May Help Explain the Link

The researchers also uncovered evidence of a biological mechanism that could help explain the association.

Their work points to a metabolic pathway involving the attachment of sugar structures to proteins. This process is a normal and important part of cell biology, but the researchers found signs that it becomes excessively active in Alzheimer's disease.

Sun said that abnormal activity in this pathway could eventually become a target for new treatments.

"Our results suggest that altered metabolism is a significant contributor to Alzheimer's progression and, in addition, addressing the metabolic defect could be an important complement to approaches focused on Alzheimer's plaques and tangles," Sun said.

Plaques and tangles are two of the best known features of Alzheimer's disease. Plaques are abnormal deposits of a protein called amyloid beta that accumulate between brain cells, while tangles are twisted forms of the tau protein that develop inside neurons. Much Alzheimer's research has traditionally focused on these abnormalities, but scientists are increasingly studying additional processes that may contribute to the disease.

Mapping Thousands of Molecules in the Brain

A spatial technology developed in Sun's laboratory helped researchers examine the metabolic changes in much greater detail.

"This technology allows us to examine thousands and thousands of molecules created when the body breaks down food or drugs and to uncover intricate pathways that otherwise would stay hidden," Sun said.

The team then focused specifically on glucosamine. Glucosamine is a naturally occurring, sugar-related molecule that can cross the blood-brain barrier, the protective boundary that tightly controls which substances can move from the bloodstream into brain tissue.

Once inside the brain, glucosamine can enter biochemical pathways that construct complex sugar structures and attach them to proteins. Commercial glucosamine supplements can be produced from materials including shellfish shells or corn.

According to the researchers, the effects of glucosamine may depend heavily on the biological environment in which it is acting. A healthy brain and a brain affected by Alzheimer's may therefore respond differently to the same molecule.

The Alzheimer's brain appeared to be particularly vulnerable to this metabolic pathway.

Mouse Experiments Point to a Possible Mechanism

To explore the mechanism more closely, the scientists studied genetically modified mice.

Glucosamine significantly increased the attachment of sugar residues to proteins inside cells. At the same time, glucosamine-treated mice developed worse deficits in "social memory" -- or memory of recognition -- compared with the other animals.

When the researchers used a chemical treatment to suppress the sugar attachment process, memory performance improved.

That experiment suggested that excessive sugar tagging could play a direct role in the memory problems seen in the animals rather than simply occurring alongside them.

Human Alzheimer's Brain Tissue Shows the Same Pattern

The researchers next examined human brain tissue with Stefan Prokop, M.D.

Brain specimens from people with Alzheimer's disease, provided by the UF Neuromedicine Brain and Tissue Bank, showed significantly more sugar attachment than tissue from normal controls.

Combined with the mouse experiments and health record analysis, the findings suggest that abnormal metabolism may be more than a secondary consequence of Alzheimer's disease. The researchers reported that it could instead contribute to the disease process itself.

"Proteins are the cell's molecular machines, and many of them need sugar tags added in just the right way to fold correctly, travel to the right place and do their jobs," Gentry said. "What we found in Alzheimer's is that this sugar-tagging system appears to be overactive. The Alzheimer's brain is adding too many of these sugar structures, and this seems to contribute to the disease rather than protect against it."

The results raise a potentially important question about glucosamine use among people with cognitive impairment or dementia, but they do not yet establish that people should stop taking the supplement. A controlled human clinical trial will be needed to determine whether glucosamine directly accelerates Alzheimer's progression and, if so, which patients may be most vulnerable.

Journal Reference:

1. Tara R. Hawkinson, Zizhen Liu, Roberto A. Ribas, Terrymar Medina, Rikke S. Nielsen, Harrison A. Clarke, Xin Ma, Angela C. Mueller, Adrielle F. Plasencia, Alexander L. Sheer, Samantha T. Simpson, Charles M. Soto, Jessica Sudderth, Feng Cai, Alex R. Cantrell, Matthieu G. Colpaert, Cameron J. Shedlock, Lei Wu, Lyndsay E. A. Young, Damon D. Kooser, Li Chen, Alison M. Ryan, Sadi Quinones, Jihye Son, Parastoo Azadi, Ralph J. Deberardinis, Stefan Prokop, Derek Allison, Shuang Yang, Hongyu Chen, Yu Huang, Xing He, Kimberly M. Alonge, Jingchuan Guo, Yi Guo, Jiang Bian, Craig W. Vander Kooi, Matthew S. Gentry, Ramon C. Sun. Hyperglycosylation is a metabolic driver of Alzheimer’s disease. Nature Metabolism, 2026; 8 (6): 1410 DOI: 10.1038/s42255-026-01538-4

Courtesy:

UF Health. "Glucosamine, a popular joint supplement, linked to faster Alzheimer’s progression." ScienceDaily. ScienceDaily, 27 September 2026. <www.sciencedaily.com/releases/2026/09/260927033754.htm>.

 

 

 

 

A massive genetic study of cat tumors reveals striking similarities to human cancer and could open new paths to treatment for both species

 

Scientists have taken a major step toward understanding cancer in cats, opening what researchers once described as a genetic "black box."

In a large international study published in Science, researchers genetically analyzed cat cancers on a scale that had not been attempted before. The work could improve cancer care for cats while also helping scientists better understand how some cancers develop in humans and other animals.

The researchers also created a freely available resource that other scientists can use to study the genetics of feline cancer.

Cancer is one of the leading causes of illness and death in cats, yet scientists have historically known far less about the genetic changes behind feline tumors than they do about cancers in humans or dogs.

Dr. Geoffrey Wood, a University of Guelph pathobiology professor and co-senior author of the study, said that gap has now begun to close.

"Despite domestic cats being common pets, there was very little known about the genetics of cancer in these animals," Wood says, "until now."

Cat and Human Cancers Share Key Genetic Changes

Researchers examined tumor samples from almost 500 domestic cats in five countries, searching for mutations and other genetic changes that help cancers form and grow.

Many cancers are driven by changes in certain genes that normally help control how cells grow, divide, repair damage, or die. When these genes are altered, cells can begin multiplying uncontrollably. Scientists often refer to genes that contribute directly to tumor growth as cancer driver genes.

The team found that many of the driver genes involved in cat cancers were also familiar from human and dog cancers.

One of the clearest examples appeared in aggressive mammary cancers, which arise in breast tissue.

The most common driver gene found in cat mammary tumors was FBXW7. More than 50 percent of the tumors examined carried a mutation in this gene.

FBXW7 normally helps regulate proteins involved in cell growth and division. When the gene is damaged, some of those growth promoting proteins can accumulate, potentially helping cancer cells survive and spread.

In humans, mutations in the FBXW7 gene in breast cancer are associated with worse prognosis - paralleling the change seen in cats.

Researchers also identified similarities between cat and human cancers affecting the blood, bones, lungs, skin, gastrointestinal system and central nervous system.

Shared Environments May Offer Cancer Clues

The similarities may be especially useful because domestic cats often live in the same environments as people.

Cats can encounter some of the same environmental factors as their owners, including household chemicals, air pollutants, smoke and other exposures that may influence cancer risk. Studying naturally occurring cancer in pets could therefore help researchers investigate how genetics and the surrounding environment interact.

"This study can help us understand more about why cancer develops in cats and humans, how the world around us influences cancer risk, and possibly find new ways to prevent and treat it," says Wood.

The genetic findings could also have implications for treatment.

Researchers found that certain chemotherapy drugs were more effective against cat mammary tumors carrying the mutated FBXW7 gene.

The result was observed only in tissue samples, so it does not yet show that the same approach will work in living cats or people. Still, the finding suggests that genetic information could eventually help doctors and veterinarians identify treatments that work better for particular tumors.

This type of approach is known as precision oncology. Instead of treating every cancer of the same general type in exactly the same way, precision oncology uses the molecular and genetic features of an individual tumor to help guide therapy.

"Having access to such a large set of donated tissues allowed us to assess drug responses across tumor types," says Dr. Sven Rottenberg, co-senior author at the University of Bern, "in a way that hasn't been possible at this scale before."

Bailey Francis, co-first author at the Wellcome Sanger Institute, said the findings could also have implications for dogs.

"When knowledge and data flows between different disciplines, we can all benefit."

Using Cat Cancer Research to Help Pets and People

The project brought together researchers from the Wellcome Sanger Institute, U of G's Ontario Veterinary College, the University of Bern and other institutions.

Rather than collecting all new samples, the team sequenced DNA from tissues that veterinarians had already obtained for diagnostic purposes.

That allowed scientists to study naturally occurring cancers from a large number of cats and compare the genetic patterns among different tumor types.

The findings also support a broader research strategy known as One Medicine.

The One Medicine approach emphasizes that human and veterinary medicine can inform one another. Cancer treatments developed for humans could potentially be evaluated in cats with naturally occurring tumors, while discoveries made during feline cancer studies and clinical trials could provide clues that help shape future human research.

That two way exchange is especially valuable because pets naturally develop many of the same diseases as people while sharing many aspects of the same environment.

Researchers hope the new genetic database will ultimately help bring more personalized cancer care to cats.

Dr. Louise Van Der Weyden, senior author at the Wellcome Sanger Institute, said the study provides a foundation for the next stage of feline cancer research.

"We can now begin to take the next steps forwards towards precision feline oncology, to catch up with the diagnostic and therapeutic options that are available for dogs with cancer, and ultimately one day, humans."

The research was funded in part by EveryCat Health Foundation, the CVS Group, Wellcome, the Natural Sciences and Engineering Research Council of Canada and the Swiss National Science Foundation.

Journal Reference:

1. Bailey A. Francis, Latasha Ludwig, Chang He, Melanie Dobromylskyj, Christof A. Bertram, Heike Aupperle-Lellbach, Hannah Wong, Aiden P. Foster, Mark J. Arends, Alejandro Suárez-Bonnet, Simon L. Priestnall, Laetitia Tatiersky, Fernanda Castillo-Alcala, Angie Rupp, Arlene Khachadoorian, Eda Parlak, Marine Inglebert, Shevaniee Umamaheswaran, Saamin Cheema, Martin Del Castillo Velasco-Herrera, Kim Wong, Ian C. Vermes, Jamie Billington, Sven Rottenberg, Geoffrey A. Wood, David J. Adams, Louise van der Weyden. The oncogenome of the domestic cat. Science, 2026; 391 (6787): 793 DOI: 10.1126/science.ady6651

Courtesy:

University of Guelph. "Scientists say house cats could help unlock better cancer treatments for humans." ScienceDaily. ScienceDaily, 26 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260924231826.htm>.

 

 

Cancer is rising in younger adults. Faster biological aging may help explain why

Younger generations may be aging faster on the inside, a biological shift researchers have linked to a higher risk of cancers diagnosed before age 55. Credit: Shutterstock

Cancer is strongly associated with age. The longer people live, the more opportunities their cells have to accumulate damage that can contribute to tumor growth. But cancer is increasingly being diagnosed in younger adults, and each newer generation appears to face a greater risk than the one before it.

That trend has prompted researchers to investigate a provocative possibility: Are younger generations accumulating biological damage more quickly, causing their bodies to age faster than expected?

A study led by researchers at Washington University School of Medicine in St. Louis offers evidence that this may be happening. The team found signs that younger generations are aging more rapidly on a biological level than older generations did at comparable ages.

Scientists are still working to understand what is driving these changes. The question is being investigated through international efforts involving research members of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute and Cancer Research U.K.

Importantly, the researchers also found that accelerated biological aging was associated with a greater risk of early-onset cancers among younger generations. In general, early-onset cancers are those diagnosed at age 55 or younger.

A Gap Between Biological Age and Actual Age

Chronological age simply measures how many years a person has been alive. Biological age, by contrast, reflects how old the body appears based on measurable changes in cells, organs, metabolism, and other physiological systems.

According to the researchers, cancer risk increased as the difference between biological age and chronological age grew. People from more recent generations tended to have larger gaps than those born earlier, suggesting their bodies appeared biologically older at the same chronological age.

That generational shift could help explain at least part of the rise in cancer among younger adults.

The team also found that aging did not appear to affect every organ system in the same way. Faster aging in specific parts of the body was associated with particular cancers. An immune system that appeared biologically older, for example, was linked to early-onset lung cancer. Older-appearing fat tissue was associated with early-onset colorectal cancer.

The findings were published in the journal Nature Medicine.

Researchers say measurements of accelerated aging could eventually help doctors identify younger people who face unusually high cancer risks, potentially allowing prevention or screening to begin earlier.

"Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalized interventions," said Yin Cao, ScD, a molecular epidemiologist and an associate professor of surgery and of medicine at WashU Medicine. "This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual's biology."

Looking Beyond Individual Cancer Risk Factors

Cao's team has previously studied numerous factors that can shape cancer risk over a person's lifetime, including obesity, metabolic dysregulation, alcohol consumption, sedentary behavior, poor diet quality and cesarean delivery.

Each of these factors can provide clues about why cancer develops at younger ages. However, no single factor appears to explain very much of the overall trend on its own.

That led Cao, who is also a research member of Siteman, and her colleagues to look for a broader way of measuring how many different influences may work together over time to increase cancer susceptibility.

Support from Cancer Grand Challenges has allowed Cao, as co-lead of Team PROSPECT, to investigate this question on a much larger scale.

For the new study, the researchers examined data from more than 154,000 young adults enrolled in the UK Biobank, which contains extensive biological, health, and lifestyle information.

They also analyzed more than 10,000 participants in the United States who are part of the National Institutes of Health's (NIH) All of Us Research Program, an initiative designed to create a comprehensive health database involving more than 1 million people living in the U.S.

Measuring How Fast the Body Is Aging

To determine biological aging, the researchers, including first author Ruiyi Tian, a doctoral student in the Cao lab, looked at two different scales.

One was systemic aging, which measures aging across the body as a whole. The other was organ-specific aging, which estimates how rapidly individual organs or biological systems are aging.

For systemic aging, the researchers relied on established approaches that use clinical biomarkers, including PhenoAge and the Klemera-Doubal Method. They also used a metabolomic age score designed to capture age-related patterns in a person's metabolism.

PhenoAge, for example, uses nine blood biochemistry markers to estimate biological aging. These include albumin, made by the liver, and creatinine, a waste product removed by the kidneys.

For organ-specific aging, the researchers analyzed blood proteomic data, which measure levels of numerous proteins associated with specific organ systems. Those protein patterns were then used to estimate the biological age of individual organs.

The team calculated the average difference between biological and chronological age within each birth cohort. They then used standard deviation to measure how far each group differed from the overall study average. Standard deviation is a measure of how spread out data points are around the average.

Younger Generations Show Older Biological Profiles

The generational differences were apparent in both the UK and U.S. populations.

Among UK participants, people born between 1965 and 1974 had systemic aging that was 23% of one standard deviation higher than people born between 1950 and 1954, even after chronological age was taken into account.

Put more simply, members of the younger generation tended to have slightly older biological profiles than members of the older generation when researchers compared them at the same chronological age.

An even larger difference appeared in the U.S. data.

Participants born between 1990 and 1999 had systemic aging that was 92% of one standard deviation higher than those born between 1965 and 1969.

The researchers then examined whether these biological aging differences were connected to cancer.

Faster Aging Linked to Early-Onset Cancer

Greater systemic aging in the younger group was associated with an 8% increased risk of early-onset solid cancers. The strongest associations involved lung, gastrointestinal, and uterine cancers.

When the participants were separated into three groups according to their level of systemic aging, another pattern emerged.

People with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared with participants showing the least advanced aging.

The association remained even after researchers accounted for inherited genetic cancer risks and genetic susceptibility to accelerated aging.

Looking at individual biological systems revealed more specific connections.

Advanced immune system aging was associated with a higher risk of early-onset lung cancer. Advanced adipose (fat) tissue aging was linked to a higher risk of early-onset colorectal cancer.

"If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions," Cao said.

Searching for the Causes of Cancer in Younger Adults

The research is part of Team PROSPECT, a Cancer Grand Challenges team co-led by Cao.

Cancer Grand Challenges is an international research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI). It brings together scientists from different specialties and countries to investigate some of the most difficult problems in cancer research.

One of those problems is explaining why early-onset cancers are becoming more common.

"Right now, we don't have a definitive answer to what's driving the rise of early-onset cancers around the world, but studies like this are helping us piece together the bigger picture, showing that cancer may be influenced not just by changes inside individual cells, but by wider changes happening across the body as a whole," said David Scott, PhD, director of Cancer Grand Challenges. "Research on this scale is possible through Cancer Grand Challenges, which brings together scientists from different fields around the world to tackle these complex questions together."

Cao and her colleagues are now working to better understand why cancer is increasingly affecting younger generations.

A major focus is determining how changes in the environment, lifestyle and society may leave long-lasting biological marks on the body. Those effects could include accelerated aging as well as other signs that make some people more vulnerable to disease.

By tracing how these risks accumulate throughout life, researchers hope to uncover more of the biological origins of early-onset cancers.

The ultimate goal is not simply to understand why cancer develops earlier, but to identify people at elevated risk while they are still healthy. That could make it possible to move prevention and screening earlier and tailor interventions to an individual's biology, shifting cancer care toward stopping disease before it begins.

This work was part of the PROSPECT team supported by the Cancer Grand Challenges initiative funded by Cancer Research UK, grant numbers CGCATF-2023/100043 and CGCATF-2023/100037; the National Cancer Institute of the NIH, grant numbers OT2CA297577 and OT2CA297576; the French National Cancer Institute; and the Bowelbabe Fund for Cancer Research UK. The project was also supported by grants from NIH/National Cancer Institute, grant number R37CA246175; the NIH/National Institute of Diabetes and Digestive and Kidney Diseases, grant number P30DK052574; the Alvin J. Siteman Cancer Center through the Foundation for Barnes-Jewish Hospital. Further support was provided by a pre-doctoral fellowship in the Cancer Biology pathway supported by NIH Molecular Oncology Training Grant T32CA113275 to Washington University School of Medicine in St. Louis; the Pediatric Gastroenterology Research Training Program grant T32DK077653 to Washington University School of Medicine in St. Louis; the Washington University School of Medicine in St. Louis Institute of Clinical and Translational Sciences, grant number UL1TR002345; and the Foundation for Barnes-Jewish Hospital. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Journal Reference:

1. Ruiyi Tian, Xiaoyu Zong, Duo Ren, Stefani Tica, Daniel Hong, Oluseye Oduyale, Jason D. Buenrostro, Ramaswamy Govindan, Yin Cao. Biological aging and generational shifts in early-onset cancer risk. Nature Medicine, 2026; 32 (8): 2983 DOI: 10.1038/s41591-026-04448-w

Courtesy:

WashU Medicine. "Cancer is rising in younger adults. Faster biological aging may help explain why." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913082200.htm>.

 

 

Scientists find a hidden cause of high blood pressure that routine tests can miss

A hidden nighttime hormone pattern may reveal one of the most commonly missed causes of high blood pressure. Credit: Shutterstock

A common and frequently missed cause of high blood pressure may be easier to detect with help from a wearable device that tracks hormone changes throughout the day and night.

New research published in Science Translational Medicine focuses on primary aldosteronism, a hormone disorder that may affect up to one in five people with high blood pressure. The condition is associated with an increased risk of heart disease, stroke, diabetes, and other serious health problems.

Researchers from the University of Bristol and the University of Manchester in the UK, the University of Bergen in Norway, and collaborators in Stockholm and Athens found that people with primary aldosteronism can experience bursts of hormone production both during the day and while asleep at night. Those nighttime surges are especially important because routine blood tests are rarely performed during sleep.

A Wearable Device Tracks Hormones Around the Clock

To capture these hidden changes, the research team used a portable device developed at the University of Bristol that allowed patients to have their hormone levels monitored continuously while living normally at home rather than staying in a hospital or research facility.

This type of continuous monitoring could reveal abnormalities that may be missed by conventional testing, potentially helping doctors identify hormone-related conditions earlier.

Study co-lead author Dr. Thomas Upton, Clinical Research Fellow in Automated Sampling Clinical Fellow at the University of Bristol, and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust said: "Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic. It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all.

"In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionize how we diagnose hypertension and ultimately reduce cardiovascular disease - particularly heart disease and strokes - that could have been prevented."

Measuring Hormones Every 20 Minutes

The proof-of-concept study followed 60 patients in Bristol, Bergen, Stockholm, and Athens over a 24-hour period. Hormone levels were measured every 20 minutes using a lightweight wearable device about the size of a mobile phone that attaches at the waist.

Because the device samples hormones from the skin, participants were able to continue with their usual activities, including sleeping at night, while researchers collected detailed hormone data.

The technology, known as U-RHYTHM, was adopted and further developed by the spinout company Dynamic Therapeutics in 2023.

Study senior author Dr. Eder Zavala, UKRI Future Leader Fellow at the University of Manchester, said: "By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts. This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively.

"A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure."

Why Standard Blood Tests May Miss the Disorder

Researchers used computational analysis to study changes in aldosterone, a hormone that helps control salt and water balance in the body. They also tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol.

The results suggest that current diagnostic approaches may miss some patients because aldosterone does not remain consistently elevated.

Even in some of the most severe cases, hormone levels sometimes dropped below the minimum thresholds typically used to diagnose primary aldosteronism. A single blood test taken at one moment could therefore capture a period when hormone levels appear relatively normal.

Instead of remaining constantly high, aldosterone showed repeated bursts of secretion at night while the overall day-night rhythm of hormone activity remained intact.

Nighttime Hormone Bursts Offer a New Clue

The hormone spikes came from the adrenal glands and were especially pronounced in patients whose primary aldosteronism was caused by a problem affecting only one adrenal gland rather than both.

Importantly, the unusual hormone patterns disappeared after the affected adrenal gland was surgically removed. That finding provided additional evidence that the bursts were directly associated with the disease.

Study co-author Prof Stafford Lightman, Professor of Medicine at the University of Bristol and inventor of the U-RHYTHM technology, added: "The findings suggest that clinicians may need to rethink how they look for the disorder, which the Endocrine Society clinical practice guidelines now recommend should be considered for all people with hypertension, also known as high blood pressure.

"Future diagnosis could move away from single time point blood tests and towards tracking the body's hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure."

Toward Earlier Detection of High Blood Pressure Causes

The findings raise the possibility that future testing for primary aldosteronism could rely less on a single blood sample and more on monitoring how hormones change over time.

Because the disorder can be treated and, in some cases, potentially cured, detecting it earlier could help reduce the risk of preventable cardiovascular complications.

The research was funded by EU Horizon 2020, the Trond Mohn Foundation, the UKRI Biotechnology and Biological Sciences Research Council (BBSRC), Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and Knut and Alice Wallenberg Foundation.

The findings support the University of Bristol's research 'Grand Challenge' focus on Understanding and Preventing Cardiovascular Disease and builds on NIHR-funded initiatives aimed at earlier identification of people with hypertension and other cardiovascular risk factors.

 

Journal Reference:

1. Marianne A. Grytaas, Thomas Upton, Isabella Marinelli, Paal Methlie, Marianne Øksnes, Dimitra A. Vassiliadi, Sophie Bensing, Georgina Russell, Kristian Løvås, Dimitris Margaritopoulos, Ileana R. Botusan, Katerina Simunkova, Maria Balomenaki, Katarina Berinder, Belinda Lombard, Thea Sjøgren, Ida Løvik, Bergithe E. Oftedal, Anette Heie, Grethe Å. Ueland, Olle Kämpe, Stylianos Tsagarakis, Stafford L. Lightman, Eder Zavala, Eystein S. Husebye. Tissue corticosteroid rhythms are dysregulated predominantly during sleep in primary aldosteronism. Science Translational Medicine, 2026; 18 (864) DOI: 10.1126/scitranslmed.aeb7517

Courtesy:

University of Bristol. "Scientists find a hidden cause of high blood pressure that routine tests can miss." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913081916.htm>. 

 

Scientists finally see DNA “zip” itself together for the first time

 

DNA strands zipping together. Credit: Professor Agnes Noy, University of York

DNA carries a negative electrical charge. Because objects with the same charge normally push away from each other, DNA molecules might be expected to repel one another. Yet inside living cells, DNA must sometimes come into close contact and recognize matching sequences. These interactions are essential for processes including genetic recombination and gene silencing, and they can also play a role in cancer.

Scientists have now captured a remarkably detailed view of how this happens. Using powerful atomic force microscopy, researchers watched short pieces of DNA align with extraordinary precision, matching one another groove for groove. Computer simulations then revealed what appears to make this close contact possible: positively charged metal ions can settle into the grooves of DNA and serve as tiny molecular bridges between the two molecules.

Tiny Ions Help DNA Overcome Repulsion

Professor Agnes Noy, from the School of Physics, Engineering and Technology at the University of York, co-led the research. She said: "This discovery could help researchers identify regions of the genome specially involved in DNA pairing. These regions may become particularly important when mutations disrupt normal cellular processes and contribute to cancer."

The results provide experimental support for an idea proposed about twenty years ago called the "DNA zipper" model. Professor Alexey Kornyshev from Imperial College London and his collaborators originally suggested that salt ions surrounding DNA could produce alternating patterns of electrical charge. Those patterns, according to the model, would help neighboring DNA molecules align with one another much like two interlocking spiral staircases.

Until now, directly observing this proposed mechanism had proved difficult.

Scientists Put the "DNA Zipper" to the Test

To investigate the process, the researchers scanned DNA samples with atomic force microscopy, a technique capable of mapping surfaces at extremely small scales. These scans allowed the team to construct detailed topographical maps showing how the DNA molecules were positioned.

At the same time, sophisticated computer simulations followed individual atoms and ions as they moved around the DNA. Combining the two approaches gave researchers both a direct view of DNA pairing and a way to understand the molecular forces responsible for it.

The simulations showed that double-charged metal ions can effectively behave like two charged arms. Each ion can interact with both DNA molecules at once, forming a bridge across the space separating them and helping hold the two strands in alignment.

Dr. Thomas Catley, co-lead author from the School of Chemical Materials and Biological Engineering at the University of Sheffield, said: "It was incredible to be able to directly visualize the long-hypothesized mechanism for the first time. The advanced imaging techniques at our disposal are allowing us to uncover these key DNA interactions which have implications in many key cellular processes."

Dr. Victor Velasco-Berrelleza from the University of Sheffield, who performed the simulations, added: "Microscopy shows us what happens, but the simulations allow us to uncover the molecular mechanism behind it."

Some DNA Sequences Pair More Strongly

The researchers also found that DNA does not pair equally well along every sequence. Some stretches of DNA created much stronger contacts than others, producing distinct hotspots where two helices were especially likely to line up.

That finding could help researchers pinpoint parts of the genome that are particularly involved in DNA recognition and pairing. Such regions may become especially significant when mutations interfere with normal cellular activity and contribute to cancer.

The discovery could also have uses beyond medicine. Because some DNA sequences can be programmed to interact more strongly than others, scientists may eventually be able to take advantage of these properties to build customized DNA structures for biotechnology.

The study, "Imaging and mechanism of DNA-DNA recognition mediated by divalent ions," was published in the journal Nucleic Acids Research.

 

Journal Reference:

1. Thomas E Catley, Victor Velasco-Berrelleza, Daniel E Rollins, Alice L B Pyne, Agnes Noy. Imaging and mechanism of DNA–DNA recognition mediated by divalent ions. Nucleic Acids Research, 2026; 54 (16) DOI: 10.1093/nar/gkag817

Courtesy:

University of York. "Scientists finally see DNA “zip” itself together for the first time." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260909231717.htm>. 

 

Your sleep may be hiding an early clue to Alzheimer’s

 Could subtle changes during sleep reveal vulnerability to Alzheimer's disease years before memory problems become noticeable? Researchers at ULiège, supported by the Stop Alzheimer's Foundation, are investigating whether the sleeping brain may contain early clues.

Scientists from the University of Liège (GIGA Neurosciences) examined sleep patterns in more than 500 healthy people. Among participants in middle age, more frequent nighttime micro awakenings were associated with a higher genetic risk of developing Alzheimer's disease. That relationship was not detected among younger adults.

The findings, published in the journal Sleep, raise the possibility that sleep measurements could eventually help researchers identify people who may be more vulnerable to Alzheimer's before symptoms develop.

Looking for Alzheimer's Clues Before Symptoms

Researchers have spent years investigating connections between disturbed sleep and neurodegenerative diseases. The University of Liège study adds another piece to that research by suggesting that the relationship between sleep and Alzheimer's risk may begin well before recognizable symptoms emerge.

Because genetics play a partial role in Alzheimer's disease (Alzheimer's disease is neither purely hereditary nor entirely independent of genes), the researchers calculated a polygenic risk (i.e., summarizing the combined influence of your genes on your probability of developing a given disease in a single figure) for more than 500 healthy participants.

Most were young adults (aged 18 to 31), while the study also included an older group (aged 50 to 69). Importantly, the polygenic risk measured in the study remained low and cannot determine whether any particular person will eventually develop Alzheimer's disease.

The researchers then compared these genetic risk estimates with different characteristics of each participant's sleep.

Tiny Awakenings During the Night

The analysis revealed an association between genetic risk for Alzheimer's disease and the frequency of nighttime micro awakenings. These are very brief bursts of brain activity that can interrupt the normal sleep cycle without causing someone to become fully awake.

Among the younger participants, researchers found no connection between these micro awakenings and Alzheimer's genetic risk. A different pattern appeared in the older group. Participants who experienced more frequent micro awakenings also tended to have higher genetic risk, despite being healthy, relatively young and free of Alzheimer's symptoms.

"These micro-awakenings are therefore not insignificant," emphasizes Puneet Talwar, a researcher at the GIGA ULiège laboratory, "certain profiles could promote the accumulation of proteins involved in Alzheimer's disease and be associated with increased vulnerability."

A Tiny Brain Region Draws Attention

The researchers also examined the locus coeruleus, a tiny area deep within the brainstem that is roughly the size of a grain of rice. It plays an important role in regulating wakefulness, attention, and sleep.

"This region is difficult to observe, but it appears to play a role in the early mechanisms linked to the disease," explains Gilles Vandewalle, co-director of the GIGA CRC In Vivo Imaging technology platform and Fund for Scientific Research - FNRS Research Director at ULiège.

In 2025, a preliminary study carried out with the 7-Tesla MRI scanner at the ULiège platform allowed the team to examine the locus coeruleus in greater detail. The researchers found that characteristics of sleep quality (speed of falling asleep, depth) were associated with the condition of the brainstem beginning at a young age.

They also found that healthy functioning of the locus coeruleus was related to the quality of REM sleep, a stage of sleep that plays an important role in memory.

The locus coeruleus is especially interesting to Alzheimer's researchers because it is among the earliest brain regions where abnormal protein deposits can appear. Such deposits may begin accumulating as early as adolescence, although scientists still do not fully understand what these early changes mean.

Could Sleep Become an Early Alzheimer's Marker?

Taken together, the findings point toward possible new approaches for Alzheimer's screening and prevention. In the future, analyzing sleep could potentially complement other methods for identifying people who may be vulnerable to the disease before symptoms become apparent.

"Sleep could become an accessible marker for the early identification of vulnerable individuals," adds Gilles Vandewalle.

Researchers are also interested in whether improving sleep could eventually help prevent or slow disease progression among people with a genetic predisposition to Alzheimer's.

"This research shows that sleep is not only an indicator of health, but also a potential lever for intervention," adds Lucie Leroux, head of French-speaking activities at the Stop Alzheimer's Foundation.

More than 220,000 people in Belgium are affected by Alzheimer's disease. For now, however, the new findings show statistical associations rather than proof that particular sleep patterns cause or predict the disease. Additional research will be needed to confirm the results, and the findings cannot currently be used to determine whether an individual will develop Alzheimer's.

Even so, the research provides another glimpse into changes that may occur long before Alzheimer's becomes clinically visible and underscores the value of basic research aimed at understanding and, eventually, anticipating the disease.

Journal Reference:

1. Nasrin Mortazavi, Puneet Talwar, Ekaterina Koshmanova, Roya Sharifpour, Elise Beckers, Alexandre Berger, Islay Campbell, Ilenia Paparella, Fermin Balda, Ismael Dardour Hamzaoui, Christian Berthomier, Christine Bastin, Christophe Phillips, Pierre Maquet, Fabienne Collette, Mikhail Zubkov, Laurent Lamalle, Gilles Vandewalle. REM sleep quality is associated with balanced tonic activity of the locus coeruleus during wakefulness. Journal of Biomedical Science, 2025; 32 (1) DOI: 10.1186/s12929-025-01127-9

Courtesy:

University of Liège. "Your sleep may be hiding an early clue to Alzheimer’s." ScienceDaily. ScienceDaily, 28 August 2026. <www.sciencedaily.com/releases/2026/08/260828005218.htm>. 

 

 

 

 

 

 

A cancer therapy put severe rheumatoid arthritis into remission

 Immunotherapies such as CAR T-cell therapy were originally developed mainly to fight cancer. But scientists are now investigating whether these personalized treatments, made from a patient's own immune cells, could also help treat or even potentially cure autoimmune diseases.

Researchers at Charité - Universitätsmedizin Berlin have now tested CAR T-cell therapy in six people with particularly severe rheumatoid arthritis. The world's first clinical trial of its kind, reported in Nature Medicine, produced encouraging early results. Disease activity fell substantially in every participant, and by the end of the observation period, three patients no longer needed rheumatoid arthritis medication.

Why Rheumatoid Arthritis Can Be So Difficult To Treat

Rheumatoid arthritis is a chronic autoimmune disease in which the immune system mistakenly attacks the joints. Repeated inflammation causes swelling and can eventually damage the joints.

Existing medications are often effective at controlling inflammation, but they generally do not cure the disease. As a result, many patients need lifelong treatment with anti-inflammatory drugs and medications that suppress the immune system, which can also cause side effects.

For some people, even newer therapies do not work well enough. Doctors describe these cases as treatment-refractory rheumatoid arthritis. Patients can continue to experience pain, limited mobility, and major reductions in quality of life despite trying multiple treatments.

"One reason could be disease-driving B cells - memory cells of the adaptive immune system that may survive in the lymph nodes, bone marrow or joint tissue after an infection, where they produce harmful antibodies directed against the body's own tissues and repeatedly reignite the inflammation," explains Prof. David Simon, who designed the trial for this patient group together with Prof. Gerhard Krönke at Charité's Department of Rheumatology and Clinical Immunology.

The researchers are testing whether CAR T cells can seek out these disease-driving B cells even when they are buried deep within body tissues. Their goal is to eliminate as much of the abnormal B-cell memory as possible and effectively give the B-cell system a new start.

Using Cancer Immunotherapy To Reset the Immune System

CAR T cells were first developed as a cancer treatment, but their potential uses are expanding. In cancer therapy, a patient's immune cells are modified so they can recognize and destroy tumor cells. For autoimmune diseases, scientists instead want to direct those engineered cells toward immune cells that help sustain the disease.

"The identifying marker on many B cells, both abnormal B cells in cancers of the blood or lymphatic system and disease-driving B cells in rheumatoid arthritis, is the surface molecule CD19. You could think of it as a kind of 'name tag'," explains David Simon. "To enable CAR T cells to detect and eliminate the disease-causing cells, we equip patients' own immune cells with a receptor that acts like a search sensor for CD19."

To produce this form of CD19 CAR T-cell therapy, doctors first collect T cells from the patient's blood. T cells are immune cells that normally help recognize and destroy infected or abnormal cells.

Scientists then genetically modify those T cells in the laboratory. The cells receive a chimeric, or artificial, antigen receptor known as a CAR, which is designed to bind specifically to CD19.

Before receiving the modified cells, patients undergo a short course of preparatory chemotherapy. This temporarily lowers the number of certain immune cells, creating room for the CAR T cells to multiply and function effectively.

The engineered cells are then returned to the patient in a single infusion. Once inside the body, they search for cells carrying CD19 and attack them. This temporarily removes all CD19-positive B cells, including long-lived disease-driving cells in the joints that can otherwise be difficult to reach. By clearing out those cells, the treatment may allow the immune system to reset.

First Trial in Severe Rheumatoid Arthritis

For the first clinical trial evaluating both the safety and effectiveness of CD19 CAR T-cell therapy in rheumatoid arthritis, the Charité team initially enrolled six patients with especially severe disease.

The group included three women and three men between the ages of 31 and 69. During the previous decade, they had received as many as eight targeted or biologic therapies, but none had controlled their disease adequately.

Researchers wanted to learn whether CAR T cells could reach the disease-driving B cells inside the joints and whether the approach could do so safely.

The first phase of the COMPARE trial produced results the team considers highly encouraging.

"Disease activity decreased markedly in all six patients. During follow-up of up to one year, three patients were in sustained remission without any medication for rheumatoid arthritis," reports Gerhard Krönke, who leads the joint Clinical Rheumatology research group at Charité and the German Rheumatology Research Center (DRFZ), a Leibniz Institute. "This is particularly remarkable given that none of the established treatments had previously been able to relieve their symptoms adequately."

CAR T Cells Reached Hidden Disease Reservoirs

The treatment appeared to do more than temporarily reduce inflammation in the joints. Researchers found that the modified immune cells also reached and eliminated disease-promoting B cells in deeper locations, including the bone marrow, lymph nodes, and joint tissue.

During regular follow-up visits over the following 12 months, levels of the autoantibodies associated with rheumatoid arthritis dropped sharply.

David Simon adds: "When the B-cell system later recovered, predominantly naïve B cells that had not yet been shaped by the disease returned. In contrast, the B cells directed against the body's own tissues that had been present before treatment were no longer detectable in almost all patients, an indication that the treatment may indeed be able to reset the pathological immune memory."

Importantly, antibodies generated by earlier vaccinations, including those against chickenpox and tetanus, could still be detected. That suggests protective antibody memory was largely preserved even though the therapy caused a profound temporary depletion of B cells.

Researchers still need to determine whether the therapy has any longer-term effects on the immune system.

Promising Results, but the Therapy Remains Experimental

The trial suggests that a single CAR T-cell treatment can, in some patients, produce a sustained period without symptoms or rheumatoid arthritis medication. This state of disease inactivity is known as remission.

For carefully selected patients whose rheumatoid arthritis does not respond adequately to available treatments, researchers hope it may eventually be possible to directly reset pathological immune memory and stop the ongoing inflammation rather than continuously suppressing it with medication.

However, CAR T-cell therapy for autoimmune diseases, including rheumatoid arthritis, is still experimental. Researchers do not yet have long-term experience with the treatment.

Responses also differed among the six participants. Some did not achieve a complete response, and one patient's disease returned after an initial period of medication-free remission.

So far, however, the researchers consider the safety findings encouraging.

"After the participants received the CD19 CAR T cells, we observed only a temporary, mild-to-moderate cytokine release syndrome (CRS) in all participants, which was readily manageable. There were no severe neurological complications or other serious adverse events, and infections were rare," explains Dr. Marie Luise Hütter-Krönke, Medical Director of the Hematology Early Clinical Trial Unit at Charité's Department of Hematology, Oncology and Cancer Immunology.

A Larger Comparison Is Next

The second phase of the trial will include ten additional patients. Researchers plan to compare CAR T-cell therapy with an already approved rheumatoid arthritis drug that also targets B cells.

The comparison should help determine whether CAR T cells produce stronger or longer-lasting effects and whether they truly reset immune memory.

If these results are confirmed in this phase and in future larger studies, CAR T-cell therapy could eventually offer another option for people with severe rheumatoid arthritis whose lives are significantly affected by the disease and who currently have no adequate treatment.

About the Study

The first of the two phases of the COMPARE study was designed to assess the safety and effectiveness of CD19 CAR T-cell therapy in treatment-refractory rheumatoid arthritis.

Major contributors included researchers from Charité's Department of Rheumatology and Clinical Immunology and the Department of Hematology, Oncology and Cancer Immunology at Campus Benjamin Franklin, along with scientists from the Cluster of Excellence ImmunoPreCept, the German Rheumatology Research Center (DRFZ), a Leibniz Institute, and the Fraunhofer Institute for Translational Medicine and Pharmacology ITMP.

The study was initiated and designed at Charité and also received support from Kyverna Therapeutics. The immunotherapy company had no role in designing the study, collecting or analyzing the data, or presenting the results.

Journal Reference:

1. Fredrik N. Albach, Marie C. Rehm, Marie Luise Hütter-Krönke, Thanh Hang Le, Julia M. Giezen, Murat Torgutalp, Arne Sattler, Ioanna Minopoulou, Robert Biesen, Edgar Wiebe, Vincent Casteleyn, Thorben Witte, Christian Furth, Jan Zernicke, Melanie Nuesch Germano, Johan Verhagen, Artur Wilhelm, Maria Dzamukova, Klaus Engel, Simon Schallenberg, Aimo Kannt, Nicole Ziegler, Michaela Fehringer, Udo Schneider, Nadine Unterwalder, Mark Beling, Alexander Pfeil, Elpida Phithak, Martin Krusche, Olaf Penack, Tobias Alexander, Werner Stenzel, Manfred Wuhrer, Kamran Movassaghi, Thomas Dörner, Eicke Latz, Thomas Vogl, Antonia Busse, Georg Schett, Hans Ulrich Scherer, Rene E. M. Toes, Arnd Kleyer, Ulrich Keller, Lars Bullinger, David Simon, Gerhard Krönke. CD19 CAR T cell therapy for treatment-refractory seropositive rheumatoid arthritis: a phase 1 trial. Nature Medicine, 2026; DOI: 10.1038/s41591-026-04603-3

Courtesy:

Charité - Universitätsmedizin Berlin. "A cancer therapy put severe rheumatoid arthritis into remission." ScienceDaily. ScienceDaily, 29 August 2026. <www.sciencedaily.com/releases/2026/08/260828082330.htm>. 

 

 

 

 

 

Researchers unveil sustainable spirulina solution to vitamin B12 deficiency

Scientists have found a way to grow Spirulina that produces biologically active vitamin B12 at levels comparable to beef, potentially overcoming one of the biggest nutritional limitations of this widely promoted algae.

The research, published in the scientific journal Discover Food, was led by Dr. Asaf Tzachor, Founder and Academic Director of the Aviram Sustainability and Climate Program at Reichman University, together with researchers from Iceland, Denmark and Austria. Using advanced biotechnology and carefully controlled light conditions, the team produced carbon-neutral, nutrient-rich Spirulina biomass containing active vitamin B12. According to the researchers, this is the first time biologically active vitamin B12 has been reported in Spirulina.

A Global Vitamin B12 Problem

Vitamin B12 is an essential micronutrient involved in several critical processes in the body, including red blood cell formation and normal nervous system function. More than a billion people worldwide are estimated to have low levels of the vitamin.

For many people, meat and dairy products are important dietary sources of B12. The recommended intake cited by the researchers is 2.4 µg/day. However, producing animal-based foods at the scale required to meet global demand also carries environmental costs, which has driven interest in more sustainable alternatives.

Spirulina blue green algae (Arthrospira platensis) has often been promoted as one such option because it is nutrient dense and can be cultivated with a relatively small environmental footprint. But there has been a major obstacle.

Traditional Spirulina contains much of its B12 in the form of pseudo-vitamin B12. Although chemically similar to the vitamin humans need, this form is not bioavailable to people, meaning the body cannot effectively use it. That limitation has prevented conventional Spirulina from serving as a reliable replacement for animal-sourced vitamin B12.

Using Light to Change Spirulina's Nutrition

To address that problem, researchers from Reichman University, University of Natural Resources and Life Sciences, Vienna, Ruppin Academic Center, Danish Technological Institute, and MATIS, Iceland, carried out an exploratory study of a biotechnology platform developed by VAXA Technologies in Iceland.

The team examined the system's engineering design, its inputs (such as energy), and the nutritional composition of the biomass it produced.

A central feature of the technology is photonic management (modified light conditions). By changing the light environment in which Spirulina grows, the researchers were able to encourage production of biologically active vitamin B12.

The cultivated Spirulina also contained other bioactive compounds associated with antioxidant, anti-inflammatory, and immune-boosting properties.

Most notably, the resulting carbon-neutral biomass contained 1.64 µg of active vitamin B12 per 100 grams, compared with 0.7-1.5 μg per 100 grams in beef.

Dr. Asaf Tzachor explains, "the findings demonstrate that photosynthetically controlled Spirulina can produce desirable levels of active vitamin B12, offering a sustainable alternative to traditional animal-source foods."

Could Spirulina Supply Vitamin B12 at Scale?

The researchers also explored what could happen if the system were expanded far beyond its current scale.

In one scenario, reallocating electricity currently used by heavy industry in Iceland could support production of 277,950 tonnes of Spirulina biomass each year. The researchers estimate that this amount would contain about 4555 grams of active vitamin B12 annually.

According to their calculations, that quantity could provide the recommended dietary allowance (RDA) for more than 13.8 million children aged 1-3.

More ambitious production scenarios could potentially supply enough vitamin B12 to meet the RDA for more than 26.5 million children aged 1-3 and more than 50 million children aged 0-6 months.

These figures are projections based on possible scale-up scenarios rather than existing production levels, but they illustrate the nutritional potential the researchers see in the technology.

A More Sustainable Source of an Essential Vitamin

If the approach can be successfully expanded, photosynthetically controlled Spirulina could provide another route for addressing vitamin B12 deficiency while reducing some dependence on meat and dairy production.

The work also highlights how biotechnology can alter the nutritional properties of microorganisms and other rapidly growing food sources. Rather than simply cultivating conventional Spirulina, researchers are changing the conditions under which it grows to encourage production of specific compounds that are useful to humans.

The findings represent a step toward developing more sustainable sources of essential nutrients, although further research and larger-scale production will be needed to determine how the technology could fit into real-world food systems.

Reichman University and the Aviram Foundation established the Aviram Sustainability and Climate Program in response to growing environmental and public health challenges around the world. The program trains students from a range of disciplines to develop strategies for addressing resource scarcity, climate change, and extreme weather events, as well as food, water, and energy crises.

 

Journal Reference:

1. A. Tzachor, S. P. van den Oever, H. K. Mayer, M. Asfur, A. Smidt-Jensen, M. Geirsdóttir, S. Jensen, B. O. Smárason. Photonic management of Spirulina (Arthrospira platensis) in scalable photobioreactors to achieve biologically active unopposed vitamin B12. Discover Food, 2024; 4 (1) DOI: 10.1007/s44187-024-00152-1

Courtesy:

Reichman University. "Researchers unveil sustainable spirulina solution to vitamin B12 deficiency." ScienceDaily. ScienceDaily, 30 August 2026. <www.sciencedaily.com/releases/2026/08/260829035227.htm>.