Medical Bulletin 26/December/2025

The findings, published in the American Journal of Gastroenterology, are being hailed as a promising step forward for those who currently face liver transplantation as their only definitive option.

PSC is a progressive disease in which the bile ducts—tubes that carry bile from the liver to the intestine—become inflamed and scarred. Over time, this scarring narrows the ducts, causing bile to build up and injure the liver. Although its exact cause remains unclear, PSC is often linked with inflammatory bowel disease (IBD), suggesting that gut-liver inflammation plays a key role. Symptoms can range from fatigue and itchy skin to jaundice, and while medications help manage discomfort, none have been proven to slow or reverse liver damage.

Nebokitug is a lab-engineered antibody that targets a molecule called CCL24, a signaling protein known to drive inflammation and scar formation in the liver. By blocking CCL24, nebokitug aims to halt the chain reaction that damages bile ducts and leads to progressive fibrosis.

To test its safety and potential benefit, researchers conducted a phase 2 randomized, placebo-controlled trial across five countries, enrolling 76 PSC patients assigned to receive one of two nebokitug doses or a placebo intravenously every three weeks for 15 weeks. The study’s primary goal was to assess safety, while secondary analyses measured liver stiffness and biomarkers associated with fibrosis.

Results were encouraging: nebokitug was well-tolerated, with only mild injection-site discomfort reported and no serious side effects or hospitalizations. Notably, patients—especially those with more advanced scarring—showed marked improvements in liver stiffness and fibrosis markers compared with placebo.

Experts say larger, long-term trials are now needed to confirm how much clinical benefit the drug can deliver—but for the first time, patients with PSC may have a real candidate for an FDA approved therapy on the horizon.

REFERENCE: Ponsioen CY, Assis DN, Boberg KM, Bowlus CL, Deneau M, Thorburn D, Aabakken L, Färkkilä M, Petersen B, Rupp C, Hübscher SG; PSC Study Group. Defining Primary Sclerosing Cholangitis: Results From an International Primary Sclerosing Cholangitis Study Group Consensus Process. Gastroenterology. 2021 Dec;161(6):1764-1775.e5. doi:10.1053/j.gastro.2021.07.046. Epub 2021 Aug 10. PMID:34384749.

Mouse study reveals surprising connection between nose-picking habit and Alzheimer’s disease

It’s a habit most people don’t think twice about — but picking your nose might do more than irritate your nasal passages. A 2022 study from Griffith University in Australia, published in Scientific Reports, uncovered a possible connection between nose picking and dementia risk, specifically Alzheimer’s disease. While the findings come from studies in mice, they raise important questions about how bacteria entering through the nose could reach the brain and trigger early processes linked to neurodegeneration.

Alzheimer’s is characterized by the buildup of amyloid beta plaques in the brain, clumps of protein long associated with memory loss and cognitive decline. The Australian research team, led by neuroscientist Dr. James St John, focused on how infection and inflammation might contribute to this process. Using a mouse model, they introduced a bacterium known as Chlamydia pneumoniae—the same species that causes pneumonia in humans—and tracked its movement through the nasal cavity.

What they found was unsettling: within 24 to 72 hours, the bacteria migrated directly from the nasal passages up the olfactory nerve into the brain, where they triggered immune responses and increased deposits of amyloid beta protein. Damage to the nasal lining made this invasion much easier. When the delicate nasal epithelium was injured — something that can happen through frequent nose picking or plucking nose hairs — the infection spread more quickly and caused heavier plaque accumulation in the mouse brains.

Dr. St John suggests this mechanism could help explain how infections act as environmental triggers for neurodegenerative diseases. The researchers emphasized, however, that the work was done in animals, and similar effects in humans still need to be confirmed.

Follow up studies will aim to test whether the same pathway exists in people and whether amyloid beta buildup in this context represents a harmful process or a protective immune response. Until then, experts advise minimizing injury to the nasal lining.

While more research is needed, the message is clear: the humble nose may hold unexpected clues to how Alzheimer’s begins — and perhaps how to prevent it.

REFERENCE: Chacko, A., Delbaz, A., Walkden, H. et al. Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk. Sci Rep 12, 2759 (2022). https://doi.org/10.1038/s41598-022-06749-9

MIT scientists develop method to remove cancer cells’ protective sugar coating

Cancer cells are masters of disguise—using sugar molecules on their surface to hide from the immune system. But scientists at MIT and Stanford University have now developed a breakthrough therapy that strips away this sugary camouflage, allowing the body’s defenses to see and destroy tumors. Their new approach, published in Nature Biotechnology, combines two powerful biological tools into one hybrid antibody lectin molecule—called AbLec—that supercharges immune responses against cancer.

Immunotherapy has revolutionized cancer treatment by teaching the immune system to recognize tumors, yet many patients still fail to respond to the most successful drugs, known as checkpoint inhibitors. These treatments block proteins like PD 1 and PD L1, which act like brakes on immune cells. However, scientists have recently discovered another lesser known “checkpoint”: sugar coated structures called glycans. Tumor cells decorate themselves with unusual glycans rich in a sugar called sialic acid, which binds to receptors named Siglecs on immune cells, silencing their attack.

Led by Dr. Jessica Stark at MIT’s Koch Institute and Nobel laureate collaborator Dr. Carolyn Bertozzi at Stanford, the researchers designed AbLecs to block this sugar based immune brake. Each AbLec links a lectin protein—which can bind sialic acids—to a tumor targeting antibody. The antibody delivers the lectin directly to cancer cells, where it locks onto the glycans and prevents them from engaging Siglec receptors, freeing macrophages and natural killer (NK) cells to attack.

In laboratory experiments, AbLecs revived immune activity against tumor cells that had previously gone undetected. In mouse models engineered with human immune receptors, a HER2 targeted AbLec significantly reduced lung metastases compared to its parent antibody, trastuzumab (Herceptin), used for breast and stomach cancers. The platform proved adaptable too—by swapping the antibody component (to drugs like rituximab or cetuximab) or altering the lectin type, the molecule can be “re wired” for multiple cancer types.

The discovery opens an exciting frontier in immunotherapy—one that targets cancer’s hidden sugar shield instead of protein switches alone. If further clinical testing confirms these results, AbLecs could become a new class of smarter, more adaptable treatments that help extend immunotherapy’s success to far more patients.

REFERENCE: Jessica C. Stark, Melissa A. Gray, Itziar Ibarlucea-Benitez, Marta Lustig, Annalise Bond, Brian Cho, Ishika Govil, Tran Luu, Megan J. Priestley, Tim S. Veth, Wesley J. Errington, Bence Bruncsics, Mikaela K. Ribi, Leo A. Williams, Casim A. Sarkar, Simon Wisnovsky, Nicholas M. Riley, Meghan A. Morrissey, Thomas Valerius, Jeffrey V. Ravetch, Carolyn R. Bertozzi. Antibody-lectin chimeras for glyco-immune checkpoint blockade. Nature Biotechnology, 2025; DOI: 10.1038/s41587-025-02884-6