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>.