Scientists finally crack an “undruggable” pancreatic cancer target and nearly double survival

 

For a long time, the likelihood of surviving pancreatic cancer has been extremely low. For patients who were diagnosed with metastatic pancreatic cancer between 2015 and 2021, about 97% died within five years of their diagnosis.

Pancreatic cancer is so deadly in part because there are no effective screening tests, and it rarely causes noticeable symptoms in its earliest stages. By the time a patient experiences signs, such as jaundice – a yellowing of the skin – or abdominal pain, the cancer has often already spread to other organs.

As a gastrointestinal oncologist and researcher specializing in early-phase clinical trials, I have seen the critical need for more effective therapies for patients with pancreatic cancer. For decades, successfully targeting the central mechanism that causes the vast majority of pancreatic cancers was considered impossible.

However, that narrative is rapidly changing with a new drug that can shut down the key protein that drives pancreatic cancer, nearly doubling survival rates for patients with advanced stages of the disease.

‘Undruggable’ tumors

The standard treatment for advanced pancreatic cancer has historically relied on chemotherapy, potent drugs designed to kill rapidly dividing cells. While chemotherapy can slow the progression of the disease, its effectiveness is often limited by the ability of pancreatic cancer cells to develop resistance against these drugs.

Pancreatic cancer’s success lies in its genetics. More than 90% of pancreatic tumors are driven by mutations in a gene called KRAS. This gene codes for proteins that function as switches that turn cell growth on and off. When the KRAS gene is mutated, the switch becomes permanently stuck in the “on” position, commanding cancer cells to multiply endlessly.

For decades, scientists considered KRAS to be “undruggable.” The surface of the protein is exceptionally smooth, lacking the molecular pockets that standard drugs require to bind to and turn the switch off.

Because existing drugs haven’t been able to target this protein, treatment for pancreatic cancer has primarily relied on toxic drugs that act more like blunt instruments than precise tools. Chemotherapy attempts to control the disease through widespread cell destruction, causing significant collateral damage to healthy tissues that lead to side effects.

What is daraxonrasib?

A new drug called daraxonrasib offers a critical advance in treating metastatic pancreatic cancer.

Daraxonrasib is taken daily by mouth. Instead of binding to KRAS directly, it attaches to a molecule called cyclophilin A in cells that helps fold proteins into their final 3D structures. This protein complex is then able to bind to the active KRAS protein and shut down its ability to signal cancer cells to multiply.

The company developing the drug, Revolution Medicines, presented results on May 31, 2026, from its Phase 3 clinical trial of 500 patients with metastatic pancreatic cancer who had received prior treatment. Compared to standard chemotherapy, daraxonrasib nearly doubled overall survival from 6.7 months to 13.2 months after diagnosis. Overall, daraxonrasib reduced the risk of death for metastatic pancreatic cancer patients by 60%.

The most common side effect is a prominent skin rash, which affected more than 86% of patients in the study. Patients also frequently dealt with stomatitis – painful swelling and sores inside the mouth – as well as diarrhea, nausea and vomiting. However, patients taking daraxonrasib were far less likely to stop treatment due to severe side effects compared to chemotherapy, and they had improved quality of life with reduced pain.

Next steps for daraxonrasib

By successfully targeting the specific genetic mutation that drives the vast majority of pancreatic cancers, researchers have demonstrated that this “undruggable” disease is treatable with targeted therapy.

The immediate next step is regulatory review of the drug’s readiness for the clinic. With data now officially published, Revolution Medicines will use these findings to seek formal approval from the Food and Drug Administration and other global regulatory bodies.

Because advanced pancreatic cancer is notoriously difficult to treat, breakthrough therapies that demonstrate this kind of significant survival benefit are often granted expedited or priority review. When daroxonrasib becomes available to patients will depend on the review timeline. Should the drug obtain approval, it could be available in clinics within months.

For the broader landscape of drug development, this milestone represents a likely shift in pancreatic cancer treatment. I expect more clinical trials exploring combination therapies pairing KRAS inhibitors with other drugs to prevent tumors from developing resistance to treatment.

Should daraxonrasib succeed, it could help set the stage for more precise, personalized and effective treatments for pancreatic cancer in the years to come.

Journal Reference:

1. Eileen M. O’Reilly, Zev A. Wainberg, Andrew E. Hendifar, Mitesh J. Borad, Filippo Pietrantonio, Shubham Pant, Pascal Hammel, Chiara Cremolini, Gulam A. Manji, Paul E. Oberstein, Ignacio Garrido-Laguna, Christoph Springfeld, Nilofer S. Azad, Makoto Ueno, Stephen Y. Chui, Ying Zhang, Hina Patel, Yeonju Lee, Zeena Salman, Brian M. Wolpin. Daraxonrasib or Chemotherapy in Previously Treated Metastatic Pancreatic Cancer. New England Journal of Medicine, 2026; DOI: 10.1056/NEJMoa2605555

Courtesy:

The Conversation. "Scientists finally crack an “undruggable” pancreatic cancer target and nearly double survival." ScienceDaily. ScienceDaily, 4 June 2026. <www.sciencedaily.com/releases/2026/06/260604044247.htm>.

 

Humans may have hidden regenerative powers

 

For generations, scientists have viewed the inability to regrow lost body parts as one of the fundamental limitations of humans and other mammals. While creatures such as salamanders can regenerate entire limbs, humans typically heal injuries by forming scar tissue.

New research from the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS), however, suggests that regenerative abilities may not be entirely absent in mammals. Instead, they could be hidden within the body's normal healing machinery, waiting to be activated under the right conditions.

"Why some animals can regenerate and others, particularly humans, can't is a big question that has been asked since Aristotle," said Dr. Ken Muneoka, a professor in the VMBS' Department of Veterinary Physiology & Pharmacology (VTPP). "I've spent my career trying to understand that."

In a study published in Nature Communications, Muneoka and colleagues describe a new two-step treatment that enabled the regeneration of bone, joint structures, and ligaments. Although the regrown tissues were not perfect replicas of the originals, the researchers believe the approach could eventually help reduce scarring and improve tissue repair after amputations.

Redirecting Healing Away From Scar Formation

When mammals are injured, the body usually responds with fibrosis. During this process, fibroblast cells quickly close the wound and create scar tissue. While this response helps prevent infection and further damage, it also limits the body's ability to rebuild what was lost.

Animals capable of regeneration follow a different path. In salamanders, for example, similar cells gather into a structure called a blastema, which serves as a foundation for new tissue growth.

"It's as if these cells can move in two different directions," Muneoka said. "They could either make a scar or make a blastema. Our research focused on redirecting the behavior of fibroblasts already present at the injury site."

To explore whether mammalian healing could be pushed toward regeneration, the research team developed a treatment that uses two well-known growth factors in sequence.

The first step involved applying fibroblast growth factor 2 (FGF2) after the wound had already healed over. By waiting until the initial healing process was complete, the researchers allowed the body to respond normally before intervening.

According to Muneoka, the team then "changed what happens next."

FGF2 encouraged the formation of a blastema-like structure, something that does not typically occur in mammals after this type of injury. Several days later, the researchers applied a second growth factor, bone morphogenetic protein 2 (BMP2), which prompted those cells to begin building new tissues.

"This is really a two-step process," Muneoka said. "You first shift the cells away from scarring, and then you provide the signals that tell them what to build."

Rethinking the Role of Stem Cells

One of the study's most important findings is that regeneration may not require adding stem cells from outside the body, an approach commonly explored in regenerative medicine.

"You don't have to actually get stem cells and put them back in," Muneoka said. "They're already there -- you just need to learn how to get them to behave the way you want."

Dr. Larry Suva, another VTPP professor involved in the study, said the results challenge long-standing assumptions about what mammalian cells are capable of doing.

"The cells that we thought to be unprogrammable, in fact are," Suva said. "The capacity is not absent -- it's just obscured."

The researchers also found evidence that cells can be redirected to create structures outside their usual location. This process, known as positional re-specification, is an important part of development.

In practical terms, cells that would normally help form one type of tissue can be instructed to rebuild a different structure following an injury.

Regrowing Bone, Tendons, Ligaments, and Joints

Although the regenerated tissues were not exact matches to the original anatomy, the researchers successfully restored all of the major structures that had been removed during amputation, including bone, tendon, ligament, and joint tissue.

The regenerated areas contained both skeletal components and connective tissues arranged in patterns resembling natural anatomy.

"We regenerated what you would expect to see at that level of injury," Muneoka said. "The structures are there -- just not in a perfect form."

The findings also suggest that regeneration depends on multiple biological pathways working together. Rebuilding tissue appears to be far more complex than activating a single mechanism.

Potential Benefits for Wound Healing

While the research remains in its early stages, the scientists believe it could have practical applications long before complete regeneration becomes possible.

Rather than focusing solely on replacing missing structures, the approach may help improve healing outcomes by reducing scar formation and enhancing tissue repair.

"People should start thinking about using these signals during the healing process," Muneoka said. "Even shifting the response slightly away from scarring could have real benefits."

The path toward clinical testing may also be more straightforward than with many experimental therapies. BMP2 already has FDA approval for certain medical applications, and FGF2 is currently being evaluated in multiple clinical trials.

A New View of Mammalian Regeneration

The study adds to growing evidence that regeneration in mammals may not be a completely lost trait. Instead, it may be a dormant capability that normally remains inactive during healing.

"This changes the way we think about what's possible," Suva said. "Once you show that regeneration can be activated, it opens the door to asking entirely new questions."

For Muneoka, those questions have driven decades of research and now have a promising new framework.

"Regenerative failure in mammals can be rescued," he said. "Now we have a model to begin figuring out how."

Journal Reference:

1. Ling Yu, Mingquan Yan, Katherine Zimmel Scaturro, Osama Qureshi, Yu-Lieh Lin, Benjamin B. Bartelle, C. Addison Smith, Daniel Osorio Hurtado, James J. Cai, Lindsay A. Dawson, Regina Brunauer, Larry J. Suva, Manjong Han, Connor P. Dolan, Ken Muneoka. Digit regeneration in mice is stimulated by sequential treatment with FGF2 and BMP2. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-72066-8

Courtesy:

Texas A&M University. "Humans may have hidden regenerative powers." ScienceDaily. ScienceDaily, 17 June 2026. <www.sciencedaily.com/releases/2026/06/260617032207.htm>.

Scientists reprogram brain immune cells to fight Alzheimer’s

Researchers in Spain and Switzerland have identified an experimental molecule that may help restore the brain's natural defenses against Alzheimer's disease. The compound, known as OLE, appears to "reprogram" microglia, the brain's immune cells, allowing them to regain some of their protective abilities.

The research was led by José Vicente Sánchez Mut of the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and Miguel Hernández University of Elche (UMH), together with Johannes Gräff of the École Polytechnique Fédérale de Lausanne (EPFL). Their findings were published in the journal Cell Death and Disease.

According to the study, OLE helps microglia surround and contain beta-amyloid plaques, reducing both their size and their harmful effects. In animal studies, the treatment also led to better performance on memory tests.

How OLE Targets Alzheimer's Disease

One of the hallmarks of Alzheimer's disease is the buildup of beta-amyloid plaques in the brain. At the same time, microglia, which normally help remove these toxic deposits, gradually become less effective. As their protective functions decline, they can contribute to damage in brain cells.

The researchers found that OLE, a molecule derived from the PM20D1 gene, can shift microglia back into a more protective state. After treatment, the cells moved toward beta-amyloid plaques and surrounded them, creating a barrier that limited contact between the plaques and nearby neurons. This reduced the plaques' toxic impact on brain tissue.

"One of the most significant findings is that we have identified a molecule capable of restoring microglia's protective function," explains Sánchez Mut. "In Alzheimer's disease, these cells become progressively impaired. Our results suggest that this process can be reversed, pointing to new therapeutic and research avenues to counteract the disease," adds the researcher, who leads the Functional Epi-Genomics of Aging and Alzheimer's Disease laboratory at the IN CSIC-UMH.

Testing OLE in Worms and Mice

To evaluate the effects of OLE, the researchers used several experimental models.

The first involved genetically modified worms (C. elegans) that produce beta-amyloid. Because these worms develop disease-related damage quickly, they provide a useful way to study toxicity. Treatment with OLE reduced the buildup of protein aggregates and improved the animals' movement, indicating a protective effect.

The team then tested the compound in mouse models of Alzheimer's disease. Mice received OLE for three months, after which researchers examined both memory and brain changes. The treated animals performed better on memory tests and showed fewer beta-amyloid plaques than untreated mice.

Microglia Show the Strongest Response

To better understand how OLE works, the researchers examined the activity of thousands of individual cells in the brain. Their analysis revealed that microglia were the cells most strongly affected by the treatment.

Following exposure to OLE, microglia activated pathways involved in clearing beta-amyloid and regained their ability to move toward plaques and contain them.

"Single-cell analysis allowed us to determine that microglia were the cells that responded most strongly to the treatment," says Victoria Pozzi, first author of the study. "From there, we observed that the compound helped these cells move toward beta-amyloid plaques and better contain the damage associated with the disease," adds the researcher.

Additional experiments in cell cultures produced similar results. Microglia treated with OLE were more effective at moving toward beta-amyloid deposits and helping remove them. In separate neuronal cultures exposed to conditions resembling those seen in Alzheimer's disease, OLE improved cell survival, suggesting the compound may also directly protect neurons.

Potential for Future Alzheimer's Therapies

The findings are covered by two European patents, including one owned by the CSIC. The researchers say this strengthens the translational potential of the work and supports future efforts to develop therapeutic applications based on the discovery.

The study received funding from the Dementia Research Switzerland -- Synapsis Foundation (Switzerland), the Pasqual Maragall Researchers Programme (PMRP) of the Pasqual Maragall Foundation, the Spanish Ministry of Science, Innovation and Universities, the Severo Ochoa Centres of Excellence programme of the State Research Agency (AEI), the Prometeo program of the Generalitat Valenciana, the European Regional Development Fund (ERDF), and the CSIC Interdisciplinary Thematic Platform PTI+ NEURO-AGING. Additional support came from the Swiss National Science Foundation, the École Polytechnique Fédérale de Lausanne (EPFL), the European Research Council (ERC), the National Research Foundation of Korea (NRF), and the European Social Fund (ESF+).

Journal Reference:

1. Victoria Pozzi-Ruiz, Aida Giner de Gracia, Liliane Glauser, Mario Romani, Fatima Gunter-Rahman, Alejandro González-Ramón, Mahmood Haj-Yahya, Rajasekhar Kolla, Allison M. Burns, Hilal A. Lashuel, Johan Auwerx, Johannes Gräff, Jose V. Sanchez-Mut. The PM20D1-OLE pathway induces microglia rewiring to ameliorate Alzheimer disease. Cell Death, 2026; 17 (1) DOI: 10.1038/s41419-026-08791-1

Courtesy:

Universidad Miguel Hernandez de Elche. "Scientists reprogram brain immune cells to fight Alzheimer’s." ScienceDaily. ScienceDaily, 19 June 2026. <www.sciencedaily.com/releases/2026/06/260619020506.htm>. 

 

AI-designed universal coronavirus vaccine passes first human trial

A new type of universal coronavirus vaccine has passed its first human clinical trial, marking an important step toward broader protection against future virus outbreaks.

Developed by researchers at the University of Cambridge and the university spinout company DIOSynVax (DVX) Ltd, the experimental vaccine was found to be safe and caused no significant side effects in a study involving 39 healthy volunteers.

Unlike conventional vaccines that target specific virus strains, this vaccine was designed to protect against multiple members of the Sarbeco coronavirus family. This group includes SARS-CoV-2, the virus responsible for the COVID-19 pandemic, as well as SARS and several related bat coronaviruses that could potentially spill over into humans in the future.

The trial showed that the vaccine stimulated immune responses not only against SARS-CoV-2 and SARS, but also against related bat viruses that have not yet infected humans.

The findings were published in the Journal of Infection.

AI Designed Vaccine Technology

The study also marked another milestone. It was the first time a vaccine whose active ingredient was created entirely through computer simulations was tested in people.

Researchers used artificial intelligence and machine learning to design what they call a "super-antigen." The antigen is the component of a vaccine that trains the immune system to recognize and fight infection.

Rather than focusing on a single virus strain, the AI system analyzed genetic information from Sarbeco coronaviruses collected through surveillance programs worldwide. Using this information, it identified features shared across the entire virus group and combined them into a single vaccine antigen.

The goal is to create protection not only against known viruses, but also against future strains that have not yet emerged.

"This trial proves the safety of an entirely new way of designing vaccines. The technology uses an AI-designed 'super-antigen' to provide lasting protection against a broad range of viruses -- for example the Ebola group, or Sarbeco coronavirus group -- even as they mutate."

Researchers believe the same strategy could eventually be applied to other virus families, including Ebola viruses and influenza viruses.

Moving Beyond Constant Vaccine Updates

Many current vaccines, including seasonal flu shots and updated COVID-19 vaccines, are designed around virus strains already circulating in people. Because viruses evolve continuously, vaccines often need regular reformulation and annual updates.

Professor Jonathan Heeney from the Lab of Viral Zoonotics in the University of Cambridge's Department of Veterinary Medicine, who led the scientific research, said the new approach could help solve that problem.

"We've converted vaccine development from being reactive to being future proof. Our vaccines will continue to provide protection against viruses even as they mutate into new strains," said Heeney.

He added: "We've overcome the problem of traditional vaccines, which have limited protection. It means we can escape the constant cycle of chasing the virus variants circulating in humans and updating the vaccines to try to catch up, like a dog chasing its tail."

By targeting features shared across an entire virus family, researchers hope the vaccine will remain effective even as new variants appear.

Human Clinical Trial Results

Volunteers between the ages of 18 and 50 received the vaccine at National Institute for Health and Care Research (NIHR) Clinical Research Facilities in Southampton and Cambridge.

The study was sponsored by University Hospital Southampton NHS Foundation Trust (UHSFT).

The vaccine's super-antigen can be used with several different vaccine delivery platforms. In this trial, researchers delivered it as a DNA vaccine using a micro fluid jet system.

Because the method does not require a needle, it could offer an alternative for people who are uncomfortable with injections. Researchers also believe it may make large scale vaccination campaigns easier and faster, particularly in settings where traditional injections are more difficult to administer.

Before human testing began, animal studies showed the vaccine could generate strong immune responses against multiple coronaviruses.

The vaccine still requires additional testing before it could become available for public use. A larger Phase 2 study is planned to evaluate immune responses in a broader and more diverse group of participants and to confirm the vaccine's ability to generate strong, wide ranging protection.

Preparing for Future Pandemic Threats

Scientists say the need for broader vaccine protection remains urgent because many potentially dangerous viruses continue to circulate in animals around the world.

"Viruses like Influenza, Coronaviruses and the Ebola group are evolving continuously and by the time vaccines are rolled out, they may be poorly matched -- the current "reactive" vaccine system struggles to keep pace," said Professor Saul Faust from the University of Southampton, the trial's chief investigator.

He added: "This new class of universal vaccines are future-proofed. They not only protect against many variants simultaneously, but potentially against related viruses that haven't yet emerged and spilt over to humans.

"If we can develop and clinically advance this new class of vaccines before a virus outbreak begins, millions of lives could be saved, lockdowns avoided and the economy preserved."

Professor Marian Knight, Scientific Director for NIHR Infrastructure, described the results as an important advance.

"The remarkable success of this AI-designed 'super-antigen' trial marks a pivotal leap forward in our ability to deliver broad, lasting viral protection."

She added: "This milestone was only made possible through partnerships between the life sciences sector and our world-class NIHR infrastructure in Cambridge and Southampton, whose Clinical Research Facilities provided the vital expertise and environment needed to safely fast-track this innovation, and bring it one big step closer to patients."

Researchers note that SARS-CoV-2 and other Sarbeco coronaviruses remain public health concerns. At the same time, many other viruses continue to circulate in animals and could potentially cross into humans, although it is impossible to predict which virus might emerge next or when.

The project was funded primarily by Innovate UK.

DIOSynVax, short for Digitally Immune Optimised Synthetic Vaccines, was founded in 2017 as a University of Cambridge spinout with support from Cambridge Enterprise, the university's commercialization arm.

The company's vaccine development pipeline also includes candidates targeting seasonal influenza, pandemic influenza threats, hemorrhagic fever viruses, and coronaviruses including SARS-CoV-2.

Jonathan Heeney is Professor of Comparative Pathology at the University of Cambridge and a Fellow of Darwin College.

Journal Reference:

1. Alasdair PS Munro, Matteo Ferrari, Rebecca Kinsley, Daniel Egan, Sneha Vishwanath, Thomas Bower, Andrew Chan, Matthew Davies, Joanne Marie M. Del Rosario, Ron Moss, Yvanne Enever, Benedict Asbach, Ralf Wagner, Rachel Bousfield, Krishna Chatterjee, Victoria Cornelius, Saul N. Faust, Jonathan L. Heeney. A phase I, needle free, dose escalation clinical trial of pEVAC-PS, a candidate pan-Sarbecovirus Vaccine. Journal of Infection, 2026; 92 (6): 106759 DOI: 10.1016/j.jinf.2026.106759

Courtesy:

University of Cambridge. "AI-designed universal coronavirus vaccine passes first human trial." ScienceDaily. ScienceDaily, 5 June 2026. <www.sciencedaily.com/releases/2026/06/260605023357.htm>.  

 

 

Popular joint supplement glucosamine linked to faster Alzheimer’s progression

A widely used supplement marketed for joint pain relief may be linked to faster progression of Alzheimer's disease, according to new research from the University of Florida.

The study found that people with mild cognitive impairment who reported taking glucosamine were more likely to progress to dementia than those who did not use the supplement. Researchers also uncovered evidence suggesting that glucosamine may interact with biological processes in the brain that are already disrupted in Alzheimer's disease.

The findings, published June 9 in Nature Metabolism, are based on a large analysis of patient health records combined with advanced imaging studies of human brain tissue and mouse models of Alzheimer's disease.

Although the results do not prove that glucosamine causes dementia and will need to be confirmed in clinical trials, researchers say the work adds to growing evidence that metabolic dysfunction plays an important role in neurodegenerative diseases.

"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 Use and Dementia Risk

Because glucosamine is widely available and frequently used by older adults to support joint health, the researchers wanted to determine whether it could influence Alzheimer's disease and related dementias (ADRD).

Working with collaborators Yi Guo, Ph.D., and Jiang Bian, Ph.D., the team used artificial intelligence to analyze deidentified UF Health records collected between 2012 and 2024. They focused on patients diagnosed with either ADRD or mild cognitive impairment (MCI).

Among those patients, researchers found that glucosamine use was relatively common. A total of 1,896 patients with ADRD and 2,750 patients with MCI reported taking the supplement, representing about 8% of each group.

After accounting for factors such as age, sex, and demographics, the analysis showed that glucosamine use was associated with a 25% greater likelihood that patients with MCI would later develop dementia.

Researchers also observed that glucosamine use was linked to a 25% increase in mortality risk among people already diagnosed with ADRD. No similar increase was seen among patients with MCI, suggesting that the supplement's effects may differ depending on the stage of disease.

A Potentially Important Metabolic Pathway

The study also pointed to a specific biological process that may help explain the association.

Researchers identified evidence that a protein and sugar-tagging pathway is excessively active in Alzheimer's disease. According to the team, this pathway could represent a new target for future 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.

The discovery was made possible by advanced spatial analysis technology developed in Sun's laboratory.

"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.

How Glucosamine Affects the Brain

To investigate further, researchers focused on glucosamine because it is a naturally occurring sugar-related molecule that can cross the blood-brain barrier. Once in the brain, it can contribute to biochemical pathways involved in building complex sugar structures on proteins. Commercial glucosamine supplements are often produced from materials such as shellfish shells or corn.

The findings suggest that glucosamine's effects may depend heavily on the biological environment in which it is acting.

"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."

According to Gentry, the Alzheimer's brain may be especially susceptible to disruptions in this pathway compared with healthy brain tissue.

Experiments in genetically modified mice provided additional support for the hypothesis.

Researchers found that glucosamine significantly increased the attachment of sugar molecules to proteins within cells. Mice receiving glucosamine also showed worsening deficits in social memory, which is the ability to recognize and remember other individuals.

When scientists chemically reduced this sugar-tagging activity, memory performance improved.

The team then examined human brain tissue from the UF Neuromedicine Brain and Tissue Bank in collaboration with Stefan Prokop, M.D. Compared with healthy control samples, Alzheimer's brain specimens showed substantially higher levels of sugar attachment to proteins.

Taken together, the researchers say these findings suggest that this metabolic abnormality may actively contribute to Alzheimer's disease rather than simply occur as a consequence of it.

"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."

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; DOI: 10.1038/s42255-026-01538-4

Courtesy:

UF Health. "Popular joint supplement glucosamine linked to faster Alzheimer’s progression." ScienceDaily. ScienceDaily, 10 June 2026. <www.sciencedaily.com/releases/2026/06/260610003044.htm>. 

 

 

Scientists crack a decades-old CO2 problem and triple fuel production

Converting carbon dioxide (CO₂) into methanol is widely viewed as a promising way to recycle carbon resources. However, scientists have long faced a difficult challenge when trying to improve the process.

At lower temperatures, converting CO2 into methanol is thermodynamically favorable. The problem is that CO2 becomes difficult to activate under these conditions, resulting in weak catalytic performance. Raising the temperature speeds up the reaction, but it also encourages a competing process known as the reverse water-gas shift reaction, which produces unwanted byproducts and lowers methanol selectivity. This persistent trade-off between catalytic activity and selectivity has limited progress in increasing methanol yields.

New Catalyst Design Overcomes Long-Standing Trade-Off

In a study published in Chem, researchers led by Prof. Jian Sun and Prof. Jiafeng Yu of the Dalian Institute of Chemical Physics (DICP) at the Chinese Academy of Sciences (CAS) developed a new catalyst design aimed at addressing this challenge.

Their approach uses a strong metal-support interaction (SMSI)-driven overlayer structure to spatially separate active sites within the catalyst. This design allows different reaction steps to occur in different locations, improving the efficiency of methanol production from CO₂.

By restructuring the catalyst surface and changing how reactants adsorb, dissociate, and move through the reaction pathway, the team achieved a space-time yield of 1.2 g·g_cat^-1·h^-1 at 300 ℃ and 3 MPa. That performance is approximately three times higher than that of conventional commercial Cu/Zn/Al catalysts.

Redirecting CO₂ Toward Methanol

The researchers found that their catalyst encourages CO₂ to adsorb and activate primarily on zirconia (ZrO₂) sites. This steers the reaction toward methanol production through the formate pathway.

In conventional Cu-based catalysts, activation typically begins by breaking the C=O bond before hydrogenation occurs. The new strategy follows a different sequence. Hydrogenation takes place first on ZrO₂ sites, and C=O bond cleavage occurs afterward.

According to the researchers, this change in reaction mechanism significantly reduces the formation of carbon monoxide (CO) byproducts while preserving the strong ability of Cu sites to dissociate H₂ efficiently.

"Our study may provide a new pathway to addressing the long-standing trade-off between activity and selectivity in methanol synthesis from CO₂," said Prof. Sun.

Journal Reference:

1. Habib Zada, Jiafeng Yu, Chuanyan Fang, Jian Sun. Disentangling the activity-selectivity trade-off in CO2 hydrogenation to methanol. Chem, 2026; 102942 DOI: 10.1016/j.chempr.2026.102942

Courtesy:

Dalian Institute of Chemical Physics, Chinese Academy Sciences. "Scientists crack a decades-old CO2 problem and triple fuel production." ScienceDaily. ScienceDaily, 14 June 2026. <www.sciencedaily.com/releases/2026/06/260613034234.htm>. 

 

 

New AI body map reveals obesity’s hidden attack on facial nerves

 

Researchers at Helmholtz Munich, Ludwig Maximilians University Munich (LMU), and several partner institutions have created an artificial intelligence (AI) system capable of mapping disease-related changes throughout an entire mouse body at cellular-level detail. Using the new platform, known as MouseMapper, the team discovered widespread inflammation and previously unknown nerve damage linked to obesity.

The study also identified similar molecular patterns in human tissue, suggesting that important aspects of obesity-related nerve damage may occur in both mice and people. The findings were published in the journal Nature.

Obesity is known to affect much more than body weight and metabolism. It can alter immune activity, disrupt nerve structures, and reshape tissues throughout the body, increasing the risk of conditions such as type 2 diabetes, cardiovascular disease, stroke, neuropathy, and cancer. Despite these widespread effects, scientists have lacked tools capable of studying disease-related changes across an entire intact body in high detail.

To address that challenge, a research team led by Prof. Ali Ertürk, Director of the Institute for Biological Intelligence (iBIO) at Helmholtz Munich and Professor at LMU, developed MouseMapper. The AI framework uses foundation-model-based deep learning algorithms to analyze massive whole-body imaging datasets.

The system can automatically identify and segment 31 organs and tissue types while also mapping nerves and immune cells throughout the body. This allows researchers to examine how diseases affect multiple organ systems at the same time in intact mice.

"MouseMapper is built on a foundation model, which means it generalizes far beyond the data it was originally trained on," says Ying Chen, co-first author of the study.

Transparent Mice and Whole-Body Imaging

To build the body maps, researchers first tagged nerves and immune cells in mice using fluorescent markers that glow under a microscope. They then used tissue-clearing methods to make the mice transparent while preserving the fluorescent signals, allowing scientists to see deep inside the body without cutting tissues apart.

Next, the team used advanced light-sheet microscopy to capture detailed three-dimensional images of entire mice. The process generated enormous datasets containing tens of millions of cellular structures from organs and tissues across the body.

MouseMapper then analyzed the images automatically, identifying anatomical regions, nerve networks, and immune-cell clusters throughout the animals.

This approach allowed the researchers to pinpoint exactly where inflammation and tissue damage appeared in organs such as fat tissue, muscle, liver, and peripheral nerves. Unlike earlier methods, scientists did not need to choose specific regions to study beforehand.

Obesity Linked to Facial Nerve Damage

To explore how obesity changes the body, the researchers fed mice a high-fat diet that produced obesity and metabolic problems similar to those seen in humans.

Using MouseMapper, the team found widespread alterations in immune-cell organization and nerve structures across the body. One of the most surprising discoveries involved the trigeminal nerve, a major facial nerve responsible for facial sensation and certain motor functions.

In obese mice, these sensory nerves showed a major reduction in branches and nerve endings, suggesting impaired nerve function. Behavioral tests supported that conclusion, showing that obese mice were less responsive to sensory stimulation compared to lean mice.

The researchers then focused on the trigeminal ganglion, which contains the cell bodies of facial sensory neurons. Through spatial proteomics analysis, they identified molecular changes linked to inflammation and nerve remodeling.

Importantly, many of the same molecular signatures were also found in trigeminal tissue from people with obesity. This suggests that the nerve-related changes observed in mice may also occur in humans.

"We revealed previously unknown structural and molecular changes in the trigeminal ganglion and its facial branches, and the same molecular signature was conserved in human tissue. This kind of finding simply cannot emerge from studying one organ at a time," says Dr. Doris Kaltenecker, senior scientist at the Institute for Diabetes and Cancer (IDC) at Helmholtz Munich and first author of the study.

A New Tool for Studying Complex Diseases

The researchers believe MouseMapper could become an important tool for studying diseases that affect many organ systems simultaneously, including diabetes, cancer, neurodegenerative diseases, and autoimmune disorders.

Unlike earlier approaches focused on individual tissues or organs, MouseMapper provides an integrated whole-body analysis system that can identify disease hotspots throughout an organism.

The team has also made the whole-body datasets publicly available online so researchers around the world can explore obesity-related changes across organs and tissues.

"Our goal is to create a comprehensive framework for understanding how diseases affect the body as an interconnected system," says Ali Ertürk. "Our long-term vision is to build truly realistic digital twins of mice in health and disease: cell-level atlases that we can query, perturb and screen in silico computationally. That would let us pinpoint the earliest changes a disease causes, design interventions to prevent them, and accelerate the discovery of new treatments while reducing the number of physical experiments we need to run."

The work was supported by the European Research Council (Consolidator Grant CALVARIA to A. Ertürk; grant 949017 to M. Rohm), the German Research Foundation (DFG) under Germany's Excellence Strategy within the Munich Cluster for Systems Neurology (SyNergy, ID 390857198, EXC 2145), DFG SFB 1052 (A9) and TR 296 (P03), the Collaborative Research Centre CRC 1744, the German Federal Ministry of Education and Research (NATON collaboration, 01KX2121, and HIVacToGC), the Vascular Dementia Research Foundation, the Nomis Heart Atlas Project Grant (Nomis Foundation), the Else-Kröner-Fresenius-Stiftung, the Edith-Haberland-Wagner Stiftung, the Helmut Horten Foundation, the EFSD and Novo Nordisk A/S Programme for Diabetes Research in Europe (to D. Kaltenecker), and the China Scholarship Council (to Y. Chen).

Journal Reference:

1. Doris Kaltenecker, Izabela Horvath, Rami Al-Maskari, Ying Chen, Zeynep Ilgin Kolabas, Luciano Hoeher, Mihail Todorov, David-Paul Minde, Saketh Kapoor, Sena Gül Turhan, Louis B. Kuemmerle, Hanno Steinke, Tim Wohlgemuth, Mayar Ali, Florian Kofler, Pauline Morigny, Julia Geppert, Denise Jeridi, Bastian Wittmann, Jie Luo, Suprosanna Shit, Carolina Cigankova, Victor Miro Kolenic, Nilsu Gür, Eren Aydeniz, Alara Yücecan, Melissa Ertürk, Laurent H. A. Simons, Chenchen Pan, Marie Piraud, Daniel Rueckert, Maria Rohm, Farida Hellal, Markus Elsner, Harsharan Singh Bhatia, Ingo Bechmann, Bjoern H. Menze, Stephan Herzig, Johannes Christian Paetzold, Mauricio Berriel Diaz, Ali Ertürk. A deep-learning framework reveals whole-body perturbations at cell level. Nature, 2026; DOI: 10.1038/s41586-026-10535-2

Courtesy:

Helmholtz Munich (GmbH). "New AI body map reveals obesity’s hidden attack on facial nerves." ScienceDaily. ScienceDaily, 23 May 2026. <www.sciencedaily.com/releases/2026/05/260522023308.htm>. 

 

 

 

 

Scientists uncover cancer-causing chemicals hidden in everyday foods

 

More people are paying close attention to what they eat, often tracking calories, exercising daily, and filling their plates with foods that seem naturally healthy, including fruits and vegetables. Yet even nutritious foods can carry hidden chemical concerns. Some contaminants can enter food from the environment, while others can form during high heat cooking methods such as heating, smoking, grilling, roasting, and frying.

Among the compounds of concern are polycyclic aromatic hydrocarbons, or PAHs (hydrophobic organic compounds comprising multiple fused aromatic rings). Some PAHs are known for their cancer causing potential, which makes reliable food testing an important part of protecting public health.

A Hidden Food Safety Challenge

Detecting PAHs in food is not simple. Conventional extraction methods, such as solid phase extraction, liquid liquid extraction, and accelerated solvent extraction, can be affordable, but they often require lengthy preparation, heavy hands on labor, and chemical intensive procedures that are not ideal for workers or the environment.

To solve these problems, scientists have been turning to a streamlined method known as QuEChERS (Quick, Easy, Cheap, Effective, Rugged, and Safe). The approach is designed to speed up sample preparation, reduce chemical use, improve recovery rates, and make food contaminant testing more practical for routine safety checks.

In a 2025 study, researchers from the Department of Food Science and Biotechnology at Seoul National University of Science and Technology, led by Professor Joon-Goo Lee, used QuEChERS to measure eight PAHs (Benzo[a]anthracene, Chrysene, Benzo[b]fluoranthene, Benzo[k]fluoranthene, Benzo[a]pyrene, Indeno[1,2,3-cd]pyrene, Dibenz[a,h]anthracene, and Benzo[g,h,i]perylene in food. The findings were published in the journal Food Science and Biotechnology.

Faster Testing With Strong Accuracy

The team used acetonitrile to extract PAHs from food samples, then tested several purification strategies involving different combinations of sorbents. The method was validated across multiple food matrices, showing strong performance. Calibration curves for all eight PAHs had R2 values above 0.99, indicating a highly linear and reliable measurement system.

Further analysis using gas chromatography and mass spectrometry showed that the limits of detection ranged from 0.006 to 0.035 µg/kg, while the limits of quantification ranged from 0.019 to 0.133 µg/kg. Recovery rates were also strong, ranging from 86.3 to 109.6% at 5 µg/kg, 87.7 to 100.1% at 10 µg/kg, and 89.6 to 102.9% at 20 µg/kg. Precision values stayed between 0.4 and 6.9% across all tested food matrices.

The study also reported that, among the foods tested, the highest PAH levels were found in soybean oil, followed by duck meat and canola oil.

Prof. Lee explains, "This method not only simplifies the analytical process but also demonstrates high efficiency in detection compared to conventional methods. It can be applied to a wide range of food matrices."

Why PAHs Matter

PAHs can form when food is exposed to high temperatures or smoke. According to the National Cancer Institute, PAHs can develop when fat and juices from meat drip onto a hot surface or open flame, creating smoke that deposits these compounds onto the food. PAHs can also form during smoking and may be found in sources such as cigarette smoke and car exhaust fumes.

The NCI notes that PAHs and related high temperature cooking compounds have caused cancer in animal studies, although human population studies have not established a definitive link between exposure from cooked meats and cancer. This uncertainty is one reason more accurate measurement tools are valuable. Better testing can help regulators, researchers, and food companies understand where contamination is occurring and how it can be reduced.

Newer Research Points to Broader Use

Since the SeoulTech study, other researchers have continued refining QuEChERS based methods for PAH detection. A 2025 study in Foods developed a modified QuEChERS method with a freeze out step and applied it to 302 retail food samples. That work found the highest concentration of four priority PAHs in Kezuribushi, a smoked and dried fish product, and identified grilled chicken feet as a possible health concern based on the European Food Safety Authority margin of exposure approach.

Another 2025 study focused on cereals and cereal based products. Researchers developed a modified QuEChERS method using Z Sep⁺ clean up and gas chromatography with tandem mass spectrometry. In 96 cereal samples and 18 cereal based products from the Romanian market, only chrysene was quantified in 17% of cereal samples, while no PAHs were quantified in the derived products.

Together, these newer findings suggest that QuEChERS based approaches are becoming increasingly useful for different food categories, from oils and meats to smoked products and cereals. They also show why food specific testing matters, since PAH levels can vary widely depending on ingredients, processing, cooking methods, and environmental exposure.

Safer Food Testing and Cleaner Labs

For the food industry, a faster and more efficient PAH testing method could improve safety management by making it easier to inspect products before they reach consumers. The approach may also reduce costs and improve working conditions by cutting down on time consuming procedures and limiting the use of hazardous chemicals.

"Our research can improve public health by providing safe food. It also reduces the use and emission of hazardous chemicals in laboratory testing," concludes Prof. Lee.

The broader takeaway is clear: food safety testing is becoming faster, cleaner, and more precise. By improving how scientists detect PAHs, methods like QuEChERS could help identify hidden contaminants, support safer food production, and reduce chemical waste in the lab.

About Professor Joon Goo Lee

Joon Goo Lee is a Professor at the Department of Food Science and Biotechnology, Seoul National University of Science and Technology. He is an expert in food regulation and safety assessment. He served as a scientific officer at Korea's Ministry of Food and Drug Safety and as a visiting researcher at FSANZ. He is a member of the National Food Sanitation Committee and an expert for the FAO/WHO JECFA. He also serves as the executive director of the Korean food safety societies. His research focuses on risk assessment and the reduction of contaminants in food, contributing to science based policies and improved public health.

Journal Reference:

1. Jihun Jeong, Minju Koo, Joon-Goo Lee. QuEChERS method development for the GC–MS analysis of polycyclic aromatic hydrocarbons in food. Food Science and Biotechnology, 2025; 34 (12): 2749 DOI: 10.1007/s10068-025-01910-2

Courtesy:

Seoul National University of Science & Technology. "Scientists uncover cancer-causing chemicals hidden in everyday foods." ScienceDaily. ScienceDaily, 22 May 2026. <www.sciencedaily.com/releases/2026/05/260522030853.htm>. 

 

 

 

 

Scientists discover a two-stage aging process that may cause cancer and arthritis

 

Researchers are offering a new way to understand why aging is so closely connected to chronic illness. In a review published in Aging-US titled "Aging as a multifactorial disorder with two stages," scientists from University College London and Queen Mary University of London describe a model suggesting that diseases linked to aging may develop through two separate but connected phases over the course of life.

The review was written by David Gems and Alexander Carver from University College London, along with Yuan Zhao from Queen Mary University of London. Their work combines ideas from evolutionary biology with findings from modern biomedical research to explain how early damage in the body may later contribute to diseases such as cancer, arthritis, and infections.

How Early-Life Damage May Shape Health Decades Later

According to the researchers, the first stage begins earlier in life when the body experiences various forms of disruption. These can include infections, physical injuries, or genetic mutations. While the body is often able to repair or contain much of this damage, some of it may remain hidden rather than being fully removed.

The second stage occurs later in life as normal genetic activity starts changing in ways that are no longer beneficial to the body. These late-life biological changes can weaken the body's ability to keep earlier damage under control. As a result, previously contained problems may gradually develop into disease.

The scientists argue that this process helps explain why many illnesses appear mainly in older adults even though their origins may trace back much earlier.

Why Diseases Like Shingles and Arthritis Appear With Age

The review highlights aging as a multifactorial process, meaning it is driven by many interacting biological factors instead of a single cause. The proposed model suggests that the combination of earlier damage and later-life genetic changes plays a major role in age-related disease.

For example, dormant viruses that remain inactive for years can become active again when the immune system weakens with age, leading to conditions such as shingles. In a similar way, injuries sustained in youth may eventually contribute to osteoarthritis as aging tissues become less resilient over time.

Inherited genetic mutations may also stay silent for decades before increasing the risk of diseases such as cancer or fibrosis later in life.

Evolutionary Biology and Aging Research

The researchers say their model builds on long-standing evolutionary theories of aging. One influential idea is that natural selection becomes weaker later in life, allowing harmful biological processes to emerge with age because they have less impact on reproduction and survival earlier in life.

The review also references studies involving the roundworm Caenorhabditis elegans. In these experiments, early mechanical damage in the worms eventually led to fatal infections in old age. The scientists suggest similar patterns may also occur in humans.

A New Framework for Healthier Aging

Overall, the review presents aging as a process shaped by multiple interacting causes that unfold over time. By separating aging into two major stages, early-life damage and later-life genetic activity, the researchers believe their framework could help guide future strategies aimed at disease prevention and healthier aging.

The findings also raise the possibility that reducing damage earlier in life or targeting harmful late-life biological changes could help lower the risk of chronic disease in older adults.

Journal Reference:

1. David Gems, Alexander Carver, Yuan Zhao. Aging as a multifactorial disorder with two stages. Aging, 2025; 17 (12): 2989 DOI: 10.18632/aging.206339

Courtesy:

Impact Journals LLC. "Scientists discover a two-stage aging process that may cause cancer and arthritis." ScienceDaily. ScienceDaily, 21 May 2026. <www.sciencedaily.com/releases/2026/05/260521072420.htm>. 

 

 

 

Scientists successfully transfer longevity gene and extend lifespan

 

Naked mole rats are not much to look at, but their biology has made them one of the most fascinating animals in aging research. These small, wrinkled rodents can live for decades, rarely develop cancer, and seem unusually protected from many of the diseases that normally arrive with age.

Researchers at the University of Rochester showed that one of those biological advantages can be moved into another mammal. By transferring a gene linked to the naked mole rat's unusually high levels of high molecular weight hyaluronic acid (HMW-HA), the team improved health and modestly extended lifespan in mice.

The work, published in Nature in 2023, suggested that at least some longevity traits that evolved in long-lived animals may be adaptable beyond the species that developed them. The genetically modified mice lived healthier lives and had an approximate 4.4 percent increase in median lifespan compared with ordinary mice.

"Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals," says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester.

Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, focused on a gene that helps produce HMW-HA. This substance is abundant in naked mole rats and has been tied to their striking resistance to cancer, inflammation, and age-related decline.

Why Naked Mole Rats Fascinate Aging Scientists

Naked mole rats are about the size of mice, yet their lifespans are extraordinary for rodents. They can live up to 41 years, nearly ten times longer than similarly sized rodents.

Their long lives are not the only reason scientists study them. As they age, naked mole rats appear to avoid many conditions that commonly affect other mammals, including neurodegeneration, cardiovascular disease, arthritis, and cancer. For decades, Gorbunova, Seluanov, and other researchers have been investigating how these animals stay so resilient.

One major clue is HMW-HA. Naked mole rats carry roughly ten times more of it than mice and humans. In earlier work, researchers found that when HMW-HA was removed from naked mole rat cells, those cells became more likely to form tumors.

That finding raised a powerful question. If HMW-HA helps naked mole rats resist cancer and age-related damage, could the same mechanism work in a different animal?

Transferring a Naked Mole Rat Longevity Gene

To test the idea, the Rochester team engineered mice to carry the naked mole rat version of the hyaluronan synthase 2 gene. This gene helps make the protein that produces HMW-HA.

All mammals have a version of hyaluronan synthase 2, but the naked mole rat version appears to be especially active. It seems to drive stronger gene expression, leading to greater production of the protective molecule.

The modified mice developed higher levels of hyaluronan in several tissues. They also showed stronger protection against spontaneous tumors and chemically induced skin cancer.

The effects were not limited to cancer resistance. The mice carrying the naked mole rat gene stayed healthier overall, lived longer than regular mice, had less inflammation in multiple tissues as they aged, and maintained better gut health.

Because chronic inflammation is one of the major biological features of aging, the reduction in inflammation was especially important. The researchers believe HMW-HA may work partly by directly influencing the immune system, although more research is needed to explain exactly how it produces such broad benefits.

A Small Lifespan Gain With Big Implications

The increase in median lifespan was about 4.4 percent, which is modest. But the larger significance is that a longevity mechanism from one mammal was successfully transferred to another.

That makes the finding more than a mouse study about a single gene. It supports the idea that nature's long-lived species may contain biological tools that can be studied, adapted, and possibly used to improve health in other animals.

"It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice," Gorbunova says. "Our next goal is to transfer this benefit to humans."

The researchers believe there may be two main ways to pursue that goal. One would be to slow the breakdown of HMW-HA in the body. Another would be to increase its production.

"We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials," Seluanov says. "We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health."

Newer Research Adds to the Naked Mole Rat Story

Since the 2023 Nature study, naked mole rats have continued to offer new clues about why they age so differently from other mammals. A 2025 study in Science reported another potential longevity mechanism involving cGAS, a protein better known for its role in immune defense. In humans and mice, cGAS can interfere with some forms of DNA repair, but the naked mole rat version appears to help cells repair DNA damage more effectively. That study found that specific changes in the naked mole rat protein improved genome stability and delayed signs of aging in experimental models.

This newer work does not replace the HMW-HA finding. Instead, it strengthens a broader pattern. Naked mole rats likely owe their unusually long, healthy lives to several overlapping defenses, including cancer resistance, inflammation control, DNA repair, and tissue protection.

For human aging research, that matters. A single molecule is unlikely to become a simple fountain of youth. But each discovery gives scientists another possible route for targeting the biological processes that drive age-related disease.

The 2023 gene transfer study remains a striking proof of concept. A survival strategy that evolved in one of nature's strangest mammals helped mice resist disease, age more smoothly, and live longer. The next challenge is determining whether those same biological tricks can be safely adapted to improve human healthspan.

Journal Reference:

1. Zhihui Zhang, Xiao Tian, J. Yuyang Lu, Kathryn Boit, Julia Ablaeva, Frances Tolibzoda Zakusilo, Stephan Emmrich, Denis Firsanov, Elena Rydkina, Seyed Ali Biashad, Quan Lu, Alexander Tyshkovskiy, Vadim N. Gladyshev, Steve Horvath, Andrei Seluanov, Vera Gorbunova. Increased hyaluronan by naked mole-rat Has2 improves healthspan in mice. Nature, 2023; 621 (7977): 196 DOI: 10.1038/s41586-023-06463-0

Courtesy:

University of Rochester. "Scientists successfully transfer longevity gene and extend lifespan." ScienceDaily. ScienceDaily, 10 May 2026. <www.sciencedaily.com/releases/2026/05/260510030948.htm>. 

 

 

 

 

A rare cancer-fighting plant compound has been decoded

 

Researchers at UBC Okanagan have uncovered the process plants use to create mitraphylline, a rare natural compound that has attracted attention for its possible cancer fighting properties.

Mitraphylline belongs to a unique class of plant chemicals known as spirooxindole alkaloids. These molecules are recognized for their unusual twisted ring structures and their powerful biological effects, including anti inflammatory and anti tumor activity.

Even though scientists have studied these compounds for years, the exact molecular steps plants use to produce them had remained unknown.

Breakthrough Discovery in Plant Chemistry

That mystery began to unravel in 2023 when Dr. Thu-Thuy Dang's team in UBC Okanagan's Irving K. Barber Faculty of Science identified the first known plant enzyme capable of twisting a molecule into the distinctive spiro shape.

Building on that earlier finding, doctoral student Tuan-Anh Nguyen led new research that uncovered two critical enzymes involved in the production of mitraphylline. One enzyme organizes the molecule into the correct three dimensional structure, while the second transforms it into mitraphylline itself.

"This is similar to finding the missing links in an assembly line," says Dr. Dang, UBC Okanagan Principal's Research Chair in Natural Products Biotechnology. "It answers a long-standing question about how nature builds these complex molecules and gives us a new way to replicate that process."

Why Mitraphylline Is So Valuable

Many promising natural compounds are found only in tiny amounts inside plants, making them difficult and expensive to recreate in laboratories. Mitraphylline is one of those rare substances. It exists only in trace quantities in tropical trees such as Mitragyna (kratom) and Uncaria (cat's claw), both members of the coffee family.

Now that researchers have identified the enzymes responsible for shaping and assembling mitraphylline, they have a clearer path toward producing the compound and related molecules in more sustainable ways.

"With this discovery, we have a green chemistry approach to accessing compounds with enormous pharmaceutical value," says Nguyen. "This is a result of UBC Okanagan's research environment, where students and faculty work closely to solve problems with global reach."

Nguyen also reflected on the experience of contributing to the breakthrough.

"Being part of the team that uncovered the enzymes behind spirooxindole compounds has been amazing," Nguyen adds. "UBC Okanagan's mentorship and support made this possible, and I'm excited to keep growing as a researcher here in Canada."

International Collaboration Fuels the Research

The project brought together Dr. Dang's laboratory at UBC Okanagan and Dr. Satya Nadakuduti's research group at the University of Florida.

Funding for the work came from Canada's Natural Sciences and Engineering Research Council's Alliance International Collaboration program, the Canada Foundation for Innovation, and the Michael Smith Health Research BC Scholar Program. Additional support was provided by the United States Department of Agriculture's National Institute of Food and Agriculture.

"We are proud of this discovery coming from UBC Okanagan. Plants are fantastic natural chemists," Dr. Dang says. "Our next steps will focus on adapting their molecular tools to create a wider range of therapeutic compounds."

Journal Reference:

1. Larissa C Laforest, Tuan-Anh M Nguyen, Gabriel Oliveira Matsumoto, Pavithra Ramachandria, Andre Chanderbali, Siva Rama Raju Kanumuri, Abhisheak Sharma, Christopher R McCurdy, Thu-Thuy T Dang, Satya Swathi Nadakuduti. A chromosome-level Mitragyna parvifolia genome unveils spirooxindole alkaloid diversification and mitraphylline biosynthesis. The Plant Cell, 2025; 37 (9) DOI: 10.1093/plcell/koaf207

Courtesy:

University of British Columbia Okanagan. "A rare cancer-fighting plant compound has been decoded." ScienceDaily. ScienceDaily, 12 May 2026. <www.sciencedaily.com/releases/2026/05/260512213836.htm>. 

 

 

 

Scientists reverse Alzheimer’s in mice with breakthrough nanotechnology

 

An international team of researchers has reported a striking Alzheimer's breakthrough in mice using specially engineered nanoparticles that do much more than deliver medicine. These microscopic particles act as drugs themselves, helping the brain restore its own natural cleaning system and dramatically reducing toxic protein buildup linked to Alzheimer's disease.

The work was led by scientists from the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital Sichuan University (WCHSU), together with collaborators in the United Kingdom. Their findings were published in Signal Transduction and Targeted Therapy.

Instead of focusing directly on damaged neurons, the scientists targeted the blood-brain barrier (BBB), a protective network of cells and blood vessels that controls what enters and leaves the brain. In Alzheimer's disease, this system gradually breaks down, allowing harmful proteins to accumulate and damaging brain function over time.

The researchers designed bioactive nanoparticles called "supramolecular drugs" to help restore this barrier and restart the brain's ability to remove waste.

Repairing the Brain's Cleanup System

The human brain uses enormous amounts of energy. In adults, it consumes around 20% of the body's total energy supply, and in children the figure can reach 60%. To meet those demands, the brain depends on an extremely dense network of blood vessels. Scientists estimate the brain contains roughly one billion capillaries, with nearly every neuron connected to its own blood supply.

Growing evidence suggests these blood vessels play a far larger role in dementia than previously thought. Many researchers now believe vascular damage is not simply a side effect of Alzheimer's disease but may actively drive its progression. Recent studies have also linked blood-brain barrier breakdown to early cognitive decline and increased buildup of toxic proteins.

Under healthy conditions, the blood-brain barrier helps clear waste products from the brain while blocking harmful substances such as toxins and pathogens. One of the most important waste proteins is amyloid-β (Aβ), the sticky material that forms plaques associated with Alzheimer's disease.

In Alzheimer's patients, the brain's waste disposal system begins to fail. As amyloid-β accumulates, neurons become damaged and memory problems worsen.

Alzheimer's Plaques Dropped Within Hours

To test the new therapy, researchers used genetically engineered mice that develop high levels of amyloid-β and progressive cognitive decline similar to Alzheimer's disease in humans.

The animals received only 3 doses of the nanoparticles. The effects appeared quickly.

"Only 1h after the injection we observed a reduction of 50-60% in Aβ amount inside the brain," explains Junyang Chen, first co-author of the study, researcher at the West China Hospital of Sichuan University and PhD student at the University College London (UCL).

The long-term results were even more dramatic. Scientists tracked the animals for months using behavioral and memory tests covering different stages of disease progression.

In one experiment, researchers treated a 12-month-old mouse (equivalent to a 60-year-old human) and evaluated it six months later. By that point, the animal was roughly comparable to a 90-year-old human. Despite its age, the mouse behaved similarly to a healthy animal with no signs of Alzheimer's-related decline.

"The long-term effect comes from restoring the brain's vasculature. We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses. But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What's remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels," said Giuseppe Battaglia, ICREA Research Professor at IBEC, Principal Investigator of the Molecular Bionics Group and leader of the study.

How the Nanoparticles Work

A major focus of the study was a protein called LRP1, which acts like a molecular transport system at the blood-brain barrier. Normally, LRP1 recognizes amyloid-β, binds to it, and moves it out of the brain and into the bloodstream for disposal.

But the process is delicate. If LRP1 binds amyloid-β too strongly, the transport machinery becomes overloaded and breaks down. If the interaction is too weak, waste removal does not occur efficiently enough. Either way, amyloid-β starts piling up in the brain.

The supramolecular nanoparticles were engineered to mimic the natural molecules that interact with LRP1. By doing this, the particles appear to "reset" the transport system, allowing amyloid-β to move out of the brain again.

Researchers say this strategy differs from many traditional Alzheimer's therapies because it focuses on repairing the brain's own infrastructure instead of simply attacking plaques directly.

That idea has gained momentum in recent years. Scientists increasingly view Alzheimer's as both a neurological and vascular disease, with disrupted blood flow and blood-brain barrier damage contributing to the spread of toxic proteins.

A Different Kind of Nanomedicine

Most nanomedicine approaches use nanoparticles as delivery vehicles to carry drugs into the body. In this case, the nanoparticles themselves are the therapy.

The research team created the particles using a bottom-up molecular engineering process that allowed them to precisely control their size and the number of ligands on their surface. This precision helped the particles interact with receptors on cell membranes in highly specific ways.

By influencing how these receptors move and function, the nanoparticles improved amyloid-β clearance and helped restore healthier blood vessel activity in the brain.

Researchers say this approach could eventually complement other Alzheimer's treatments, including anti-amyloid antibody drugs. One of the biggest problems facing current therapies is getting enough medicine across the blood-brain barrier safely and efficiently.

Other experimental technologies are also exploring ways to overcome this challenge, including ultrasound-based delivery systems, "brain shuttle" molecules, and additional nanoparticle platforms designed to cross the barrier more effectively.

What Happens Next

Although the findings are promising, the research remains in the animal-testing stage. Many Alzheimer's therapies that worked in mice have later failed in human clinical trials.

Still, experts say the study highlights an increasingly important area of Alzheimer's research: restoring the health of the brain's blood vessels and waste-removal systems.

"Our study demonstrated remarkable efficacy in achieving rapid Aβ clearance, restoring healthy function in the blood-brain barrier and leading to a striking reversal of Alzheimer's pathology," concludes Lorena Ruiz Perez, researcher at the Molecular Bionics group from the Institute for Bioengineering of Catalonia (IBEC) and Serra Hunter Assistant Professor at the University of Barcelona (UB).

The project involved researchers from the Institute for Bioengineering of Catalunya (IBEC), West China Hospital of Sichuan University, West China Xiamen Hospital of Sichuan University, University College London, the Xiamen Key Laboratory of Psychoradiology and Neuromodulation, the University of Barcelona, the Chinese Academy of Medical Sciences, and the Catalan Institution for Research and Advanced Studies (ICREA).

Journal Reference:

1. Junyang Chen, Pan Xiang, Aroa Duro-Castano, Huawei Cai, Bin Guo, Xiqin Liu, Yifan Yu, Su Lui, Kui Luo, Bowen Ke, Lorena Ruiz-Pérez, Qiyong Gong, Xiaohe Tian, Giuseppe Battaglia. Rapid amyloid-β clearance and cognitive recovery through multivalent modulation of blood–brain barrier transport. Signal Transduction and Targeted Therapy, 2025; 10 (1) DOI: 10.1038/s41392-025-02426-1

Courtesy:

Institute for Bioengineering of Catalonia (IBEC). "Scientists reverse Alzheimer’s in mice with breakthrough nanotechnology." ScienceDaily. ScienceDaily, 17 May 2026. <www.sciencedaily.com/releases/2026/05/260517030326.htm>. 

 

 

 

 

 

Scientists found the “holy grail” gene that could one day help humans regrow limbs

Scientists studying axolotls, zebrafish, and mice have uncovered a shared set of genes that could someday help researchers develop therapies for regrowing human limbs. The findings, published in the Proceedings of the National Academy of Sciences, point to a possible new direction for regenerative medicine and gene therapy.

"This significant research brought together three labs, working across three organisms to compare regeneration," said Wake Forest Assistant Professor of Biology Josh Currie, whose lab studies the Mexican axolotl salamander. "It showed us that there are universal, unifying genetic programs that are driving regeneration in very different types of organisms, salamanders, zebrafish and mice."

The project also included Duke University plastic surgeon David A. Brown, who studies digit regeneration in mice, and Kenneth D. Poss of the University of Wisconsin-Madison, whose research focuses on fin regeneration in zebrafish.

Shared Regeneration Genes Across Species

Around the world, more than 1 million amputations occur every year due to diabetes-related vascular disease, traumatic injuries, infections, and cancer, according to Global Burden of Disease statistics. Researchers expect that number to climb as populations age and diabetes becomes more common.

For years, scientists have searched for ways to move beyond prosthetic limbs and toward treatments capable of restoring natural movement, sensation, and function. This new study suggests that a group of genes known as SP genes may play a central role in that effort.

Researchers selected axolotls, zebrafish, and mice because each species offers unique insights into regeneration.

Axolotls are famous for their extraordinary ability to regrow entire limbs along with tails, spinal cord tissue, and parts of organs including the heart, brain, lungs, liver, and jaw.

Zebrafish are another powerful regeneration model because they can repeatedly regrow damaged tail fins. They are also capable of repairing the heart, brain, spinal cord, kidneys, retinas, and pancreas.

Mice were included because, like humans, they are mammals. Mice can regenerate the tips of their digits, and humans can sometimes regrow fingertips if the nailbed remains intact after injury, allowing skin, flesh, and bone to regenerate.

Currie said the team discovered that the regenerating epidermis, or skin tissue, in all three species activated two genes called SP6 and SP8. Researchers then began investigating exactly how those genes contribute to regeneration.

Biology Ph.D. student Tim Curtis Jr. participated in the work in Currie's lab, along with undergraduate Elena Singer-Freeman, a Goldwater Scholar and 2025 Wake Forest graduate in biochemistry and molecular biology.

CRISPR Experiments Reveal Key Limb Regrowth Role

The researchers found that SP8 is especially important for limb regeneration in salamanders. Using CRISPR gene-editing technology, Currie's team removed SP8 from the axolotl genome.

Without the gene, axolotls were unable to properly regenerate limb bones. Scientists observed similar problems in mice when SP6 and SP8 were missing from regenerating digits.

Using those findings, Brown's lab designed a viral gene therapy based on a tissue regeneration enhancer previously identified in zebrafish.

The therapy delivered a signaling molecule called FGF8, which is normally activated by SP8. In mice, the treatment encouraged bone regrowth in damaged digits and partially restored some regenerative abilities lost when the SP genes were absent.

Human limbs cannot naturally regenerate the way salamander limbs do, but researchers believe future therapies could potentially imitate some of the biological mechanisms controlled by SP genes.

"We can use this as a kind of proof of principle that we might be able to deliver therapies to substitute for this regenerative style of epidermis in regrowing tissue in humans," Currie explained.

Building Toward Future Human Limb Regeneration

Researchers caution that the work is still at an early stage, and far more studies will be needed before discoveries in mice could translate into therapies for humans. Even so, Currie described the research as an important foundation for future regenerative treatments.

"Scientists are pursuing many solutions for replacing limbs, including bioengineered scaffolds and stem cell therapies," Currie explained. "The gene-therapy approach in this study is a new avenue that can complement and potentially augment what will surely be a multi-disciplinary solution to one day regenerate human limbs."

Currie also emphasized the importance of collaboration between scientists working on very different animals and biological systems.

"Many times, scientists work in their silos: we're just working in axolotl, or we're just working in mouse, or just working in fish," Currie said. "A real standout feature of this research is that we work across all these different organisms. That is really powerful, and it's something that I hope we'll see more of in the field."

Journal Reference:

1. David A. Brown, Katja K. Koll, Erin Brush, Grant Darner, Timothy Curtis, Thomas Dvergsten, Melissa Tran, Colleen Milligan, David W. Wolfson, Trevor J. Gonzalez, Sydney Jeffs, Alyssa Ehrhardt, Rochelle Bitolas, Madeleine Landau, Kendall Reitz, David S. Salven, Leslie A. Slota-Burtt, Isabel Snee, Elena Singer-Freeman, Sayuri Bhatia, Jianhong Ou, Aravind Asokan, Joshua D. Currie, Kenneth D. Poss. Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors. Proceedings of the National Academy of Sciences, 2026; 123 (17) DOI: 10.1073/pnas.2532804123

Courtesy:

Wake Forest University. "Scientists found the “holy grail” gene that could one day help humans regrow limbs." ScienceDaily. ScienceDaily, 9 May 2026. <www.sciencedaily.com/releases/2026/05/260508003121.htm>.