The COVID-19 pandemic has taken a devastating toll on global health, with severe complications and immune-driven tissue damage being major concerns. A recent study published in Cell Reports reveals that the SARS-CoV-2 nucleocapsid protein can spread from infected to uninfected cells, triggering an immune response that mistakenly targets healthy cells. Researchers at the Hebrew University of Jerusalem have identified how this viral protein binds to cell surfaces and found a common anticoagulant, enoxaparin, can block this harmful interaction.

The study, led by PhD students Jamal Fahoum and Maria Billan from the Faculty of Medicine at the Hebrew University of Jerusalem, uncovers a surprising mechanism by which the SARS-CoV-2 virus causes immune-mediated tissue damage. The researchers used laboratory-grown cells, sophisticated imaging techniques, and samples from COVID-19 patients to understand how a specific viral protein attaches to healthy cells.

They discovered that this protein sticks to certain sugar-like molecules found on the surface of many cells, called Heparan Sulfate proteoglycans. When this happens, clumps of the viral protein form on these healthy cells. The immune system then mistakenly attacks these clumps using antibodies, which sets off a chain reaction that might damage both infected and healthy cells in the infected organism.

However, the researchers found that the drug enoxaparin can block the viral protein from sticking to healthy cells by taking over the spots the protein would normally bind to. In both lab experiments and when samples obtained from patients were tested in the lab, enoxaparin stopped the protein from attaching to cells and helped prevent the immune system from mistakenly attacking them.

This research sheds light on the mechanisms behind severe COVID-19 complications and immune-driven tissue damage. The findings open the door to new strategies for preventing immune-driven damage in COVID-19 and possibly other viral infections. Moreover, this study highlights the importance of collaborative efforts between clinicians and researchers in understanding the complexities of viral infections.

The authors dedicate this article to the memory of the late Prof. Hervé (Hillel) Bercovier, a gifted microbiologist, an inspiring scientist, and a great mentor. This research was supported by several research funds, including major contributions from The Edmond and Benjamin de Rothschild Foundation and The Israel Science Foundation of the Israel Academy of Science and Humanities.

Scientists at the USC Leonard Davis School of Gerontology have made a groundbreaking discovery that sheds light on the unique challenges faced by people with Down syndrome who develop Alzheimer’s disease. Their research reveals a crucial link between high levels of iron in the brain and increased cell damage, providing a potential explanation for why Alzheimer’s symptoms often appear earlier and more severely in individuals with Down syndrome.

Down syndrome is caused by having an extra third copy (trisomy) of chromosome 21, which includes the gene for amyloid precursor protein (APP). People with Down syndrome tend to produce more APP, leading to an increased risk of developing Alzheimer’s disease. In fact, about half of all people with Down syndrome show signs of Alzheimer’s by the age of 60, which is approximately 20 years earlier than in the general population.

The researchers studied donated brain tissue from individuals with Alzheimer’s, those with both Down syndrome and Alzheimer’s (DSAD), and those without either diagnosis. They found that the brains of people with DSAD had twice as much iron and more signs of oxidative damage in cell membranes compared to the brains of individuals with Alzheimer’s alone or those with neither diagnosis.

This excess iron leads to ferroptosis, a type of cell death characterized by iron-dependent lipid peroxidation. In other words, iron builds up, drives the oxidation that damages cell membranes, and overwhelms the cell’s ability to protect itself.

The researchers also discovered that lipid rafts, tiny parts of the brain cell membrane crucial for cell signaling and protein processing, had more oxidative damage and fewer protective enzymes in DSAD brains compared to Alzheimer’s or healthy brains. These lipid rafts showed increased activity of the enzyme β-secretase, which interacts with APP to produce Aβ proteins, potentially promoting the growth of amyloid plaques.

The findings have significant implications for future treatments, especially for people with Down syndrome who are at high risk of Alzheimer’s. Early research in mice suggests that iron-chelating treatments may reduce indicators of Alzheimer’s pathology. Medications that remove iron from the brain or help strengthen antioxidant systems might offer new hope.

The study was supported by various organizations, including the National Institute on Aging and Cure Alzheimer’s Fund. These findings highlight the importance of understanding the biology of Down syndrome for Alzheimer’s research and could lead to new therapeutic approaches for this vulnerable population.

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A groundbreaking patch, containing tens of millions of microscopic nanoneedles, could soon replace traditional biopsies. This innovative technology offers a painless and less invasive alternative for millions of patients worldwide who undergo biopsies each year to detect and monitor diseases like cancer and Alzheimer’s.

Biopsies are among the most common diagnostic procedures worldwide, performed millions of times every year. However, they can be invasive, cause pain and complications, and deter patients from seeking early diagnosis or follow-up tests. Traditional biopsies also remove small pieces of tissue, limiting how often and how comprehensively doctors can analyze diseased organs like the brain.

Now, scientists at King’s College London have developed a nanoneedle patch that painlessly collects molecular information from tissues without removing or damaging them. This breakthrough could allow healthcare teams to monitor disease in real-time and perform multiple, repeatable tests from the same area – something impossible with standard biopsies.

The nanoneedles are incredibly thin, measuring 1,000 times thinner than a human hair, and cause no pain or damage. For many patients, this means earlier diagnosis and more regular monitoring, transforming how diseases are tracked and treated.

Dr. Ciro Chiappini, who led the research published in Nature Nanotechnology, said: “We have been working on nanoneedles for twelve years, but this is our most exciting development yet. It opens a world of possibilities for people with brain cancer, Alzheimer’s, and for advancing personalized medicine.”

The patch is covered in tens of millions of nanoneedles that extract molecular “fingerprints” – including lipids, proteins, and mRNAs – from cells without harming the tissue. The tissue imprint is then analyzed using mass spectrometry and artificial intelligence, giving healthcare teams detailed insights into whether a tumor is present, how it’s responding to treatment, and how disease is progressing at the cellular level.

This technology could be used during brain surgery to help surgeons make faster, more precise decisions. For example, by applying the patch to a suspicious area, results could be obtained within 20 minutes and guide real-time decisions about removing cancerous tissue.

Made using the same manufacturing techniques as computer chips, the nanoneedles can be integrated into common medical devices such as bandages, endoscopes, and contact lenses. Dr. Chiappini added: “This could be the beginning of the end for painful biopsies. Our technology opens up new ways to diagnose and monitor disease safely and painlessly – helping doctors and patients make better, faster decisions.”