One possible explanation is that resilient brains are better at repairing themselves during Alzheimer’s. “Perhaps they can add new brain cells to a network that is degenerating”, the author says.
This idea is linked to a process called adult neurogenesis, which refers to the birth of new brain cells (neurons) in the adult brain. It has been well-established in other animals, but its existence in humans has been debated for years.
To study this, the team used human brain tissue from the Netherlands Brain Bank, which collects and stores donated brain samples for research. They included brains from control donors with no brain pathology, Alzheimer’s patients, and individuals with Alzheimer’s pathology who remained resilient to developing dementia.
The team focused on a small part of the brain’s memory center, likely one of the few areas where these new brain cells could form. “These cells are extremely rare, so we had to develop new ways to find them,” the author says. “We really zoomed in on the exact spot where we expected them to be.”
The team found what they were looking for: so-called “immature” neurons. These cells resemble young, not fully developed neurons. “Even at an average age of over 80, we still found these immature neurons in all groups,” the author says.
But the biggest surprise came next. While the team had expected to find much more of these cells in the resilient group than in the Alzheimer’s patients, the difference was not as big as expected.
Surprisingly, the team found that the key difference lies in how the immature neurons behave. “In resilient individuals, these cells seem to activate programs that help them survive and cope with damage,” the author says. “We also see lower signals related to inflammation and cell death.”
A new study calls for caution in using the well-known senolytic treatment of dasatinib and quercetin (D+Q), showing that it causes damage in certain regions of the brain, similar to what is observed in multiple sclerosis [1].
Stem cell senescence prevents brain repair
Multiple sclerosis (MS) is a brain disorder in which the patient’s own immune system attacks oligodendrocytes: cells in the nervous system that provide a myelin coating for neurons, which is essential for their function and survival. MS is much more common in older patients, who are also more likely to have progressive disease and a worse response to treatment.
Researchers have found that a “pencil beam” laser allows brain imaging 25 times faster than current methods. This could help scientists quickly test whether new drugs for diseases like Alzheimer’s or ALS are reaching their targets in the brain.
After a surprising discovery that overcomes a longstanding problem in fiber optics, MIT researchers demonstrated a biomedical imaging technique that is faster and more precise than other methods, which could help scientists and clinicians study new brain therapies.
In a new paper, researchers dive into the protein secretome and decrypt how peritoneal dialysis can trigger fibrosis and damage blood vessels, providing a resource that could inform efforts to limit toxicity from this lifesaving therapy.
Learn more in Science Signaling.
Secretomics uncovers cell-cell signaling networks in tissue remodeling induced by peritoneal dialysis.
Zhao et al. reveal a critical metabolic event in the transition of endothelial cells from proliferation into quiescence. This process requires robust NAMPT-mediated NAD metabolism to suppress H2O2 emanated from reprogramming mitochondria. Failure of this metabolic checkpoint impairs vascular stabilization during angiogenesis, offering novel opportunities for the treatment of hypervascular diseases.
A patient with three different autoimmune diseases has entered complete remission after undergoing an experimental treatment that effectively reset her immune system.
The 47-year-old woman in Germany previously required daily blood transfusions to manage her conditions, two of which affected her blood cells.
She was given Chimeric Antigen Receptor (CAR-) T cell therapy, which involves extracting a sample of immune cells, ‘supercharging’ them against a specific target, and returning them to the body.
When chemists design drug candidates, shape matters enormously. Many active pharmaceutical ingredients contain branched carbon structures—points where the molecular chain forks in a specific direction—that are critical to whether a molecule will bind to its biological target and whether it will be safe. The challenge is that the branched building blocks used to create these structures are not very abundant or commercially available. Now, scientists at Scripps Research have devised a new approach to building these branched molecular structures found in many medicines and materials: one that could make the early stages of drug discovery faster and more efficient.
The method, published in Science, overcomes a stubborn technical obstacle that has limited chemists’ ability to assemble complex molecules from simple, inexpensive starting materials.
“This work solves a selectivity problem that challenged us for years,” says Ryan Shenvi, professor at Scripps Research and senior author of the study. “We’ve now laid the groundwork to access iteratively branching materials that occur in metabolites, fragrances and drugs.”
As the Trump administration phases out the use of animal experimentation across the federal government, a biotech startup has a bold idea for an alternative to animal testing: nonsentient “organ sacks.”
Bay Area-based R3 Bio has been quietly pitching the idea to investors and in industry publications as a way to replace lab animals without the ethical issues that come with living organisms. That’s because these structures would contain all of the typical organs—except a brain, rendering them unable to think or feel pain. The company’s long-term goal, cofounder Alice Gilman says, is to make human versions that could be used as a source of tissues and organs for people who need them.
For Immortal Dragons, a Singapore-based longevity fund that’s invested in R3, the idea of replacement is a core strategy for human longevity. “We think replacement is probably better than repair when it comes to treating diseases or regulating the aging process in the human body,” says CEO Boyang Wang. “If we can create a nonsentient, headless bodyoid for a human being, that will be a great source of organs.”
Scientists have uncovered an unexpected way cells can generate cancer-driving proteins—by cutting RNA into shorter, functional fragments rather than following the standard blueprint. This process, newly termed as “RNA dicing,” enables the production of a truncated form of the JAK1 protein that remains highly active and can promote tumor growth, particularly when normal gene function is disrupted.
The finding challenges conventional views of how genetic information is translated and points to a previously unrecognized mechanism that could influence cancer progression and response to targeted therapies.
The process by which cells turn genes into proteins has long been understood as precise and tightly controlled. But new research shows that cells can unexpectedly cut RNA into shorter fragments that still produce functional proteins, sometimes with harmful consequences.