Vaccines may do far more than prevent infections.
The way that some inoculations train your immune system could also reduce the risk of cancer, stroke, or heart attacks, and possibly guard against dementia.
New evidence shows that the shingles vaccine is linked to slower aging, with benefits that can last for several years after vaccination.
Researching are throwing lots of ideas at the wall to see what sticks, but the U.S. just put some serious cash behind the idea of 3D bioprinting.
Researchers at the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), have found that a key protein can help to regenerate neural stem cells, which may improve aging-associated decline in neuronal production of an aging brain.
Published in Science Advances, the study identified a transcription factor in the brain, cyclin D-binding myb-like transcription factor 1 (DMTF1), as a critical driver of neural stem cell function during the aging process. Transcription factors are proteins that regulate genes to ensure that they are expressed correctly in the intended cells.
The study, led by Assistant Professor Ong Sek Tong Derrick and first author Dr. Liang Yajing, both from the Department of Physiology and the Healthy Longevity Translational Research Program at NUS Medicine, sought to identify biological factors that influence the degeneration of neural stem cell function often associated with aging, and guide the development of therapeutic approaches to mitigate the adverse effects of neurological aging.
For millions living with nerve pain, even a light touch can feel unbearable. Scientists have long suspected that damaged nerve cells falter because their energy factories known as mitochondria don’t function properly.
Now research published in Nature suggests a way forward: supplying healthy mitochondria to struggling nerve cells.
Using human tissue and mouse models, researchers found that replenishing mitochondria significantly reduced pain tied to diabetic neuropathy and chemotherapy-induced nerve damage. In some cases, the relief lasted up to 48 hours.
Instead of masking symptoms, the approach could fix what the team sees as the root problem — restoring the energy flow that keeps nerve cells healthy and resilient.
“By giving damaged nerves fresh mitochondria — or helping them make more of their own — we can reduce inflammation and support healing,” said the study’s senior author. “This approach has the potential to ease pain in a completely new way.
The work highlights a previously undocumented role for satellite glial cells, which appear to deliver mitochondria to sensory neurons through tiny channels called tunnelling nanotubes.
When this mitochondrial handoff is disrupted, nerve fibers begin to degenerate — triggering pain, tingling and numbness, often in the hands and feet, the distal ends of the nerve fibers.
Plants produce protective chemicals called alkaloids as part of their natural defenses. People have used these compounds for a long time, including in pain relief medicines, treatments for various diseases, and familiar household products such as caffeine and nicotine.
Scientists want to learn exactly how plants build alkaloids. With that knowledge, they hope to create new and improved medicine-related chemicals faster, at lower cost, and with less harm to the environment.
In a study at the University of York, researchers examined a plant called Flueggea suffruticosa, which makes an especially strong alkaloid known as securinine. As they traced how securinine is produced, the team found a surprise: a key step depends on a gene that resembles bacterial genes more than typical plant genes.
“The important part was we collected all the samples we need to address our primary questions,” Dugan said. “When we’re done drilling and we pull our equipment out, the holes collapse back in and seal themselves up.”
Now, scientists are studying the reservoir in finer detail, including any microbes, rare earth elements, pore space — which can help researchers better estimate the reservoir’s size — and the age of the sediments, which will help narrow down when it formed. More definitive results about how and when the reservoir formed are expected in about one month’s time, Dugan said.
“Our goal is to provide an understanding of the system so if and when somebody needs to use it, they have information to start from, rather than recreating information or making an ill-informed choice,” he said.
A multidisciplinary team has developed a selective compound that inhibits an enzyme tied to inflammation in people at genetic risk for Alzheimer’s, while preserving normal brain function and crossing the blood-brain barrier.
The findings are published in the journal npj Drug Discovery.
The driver is an enzyme called calcium-dependent phospholipase A2 (cPLA2). The team discovered its role in brain inflammation by studying people who carry the APOE4 gene —the strongest genetic risk factor for Alzheimer’s disease. While many people who have the APOE4 gene don’t develop the disease, those with elevated levels of cPLA2 generally do.
At first glance, some scientific research can seem, well, impractical. When physicists began exploring the strange, subatomic world of quantum mechanics a century ago, they weren’t trying to build better medical tools or high-speed internet. They were simply curious about how the universe worked at its most fundamental level.
Yet without that “curiosity-driven” research—often called basic science—the modern world would look unrecognizable.
“Basic science drives the really big discoveries,” says Steve Kahn, UC Berkeley’s dean of mathematical and physical sciences. “Those paradigm changes are what really drive innovation.”
In this report, researchers link thermogenic adipose tissue (brown/beige fat), best known for heat production, to blood-pressure control via direct fat–blood vessel communication. Using mouse models engineered to lose beige fat identity (via adipocyte-specific disruption of PRDM16), they observed elevated arterial pressure alongside perivascular remodeling, including fibrotic tissue accumulation and marked vascular hypersensitivity to the vasoconstrictor hormone angiotensin II. Mechanistically, loss of beige fat identity increased secretion of QSOX1 (quiescin sulfhydryl oxidase 1), which activated pro-fibrotic gene programs in vascular cells and promoted vessel stiffening; blocking this pathway (including genetic removal of QSOX1 in the model) restored healthier vascular signaling and function. The authors characterize this as a previously underappreciated, obesity-independent axis by which the “quality” (thermogenic vs white-like) of perivascular fat influences vascular stiffness and responsiveness to pressor signals, suggesting QSOX1 and related adipose-derived signals as potential precision targets for future antihypertensive therapies.
A mouse aorta with immunofluorescent tagging, emphasizing the close connection between vasculature and fat. (Credit: Cohen lab)
Obesity causes hypertension. Hypertension causes cardiovascular disease. And cardiovascular disease is the leading cause of death worldwide. While the link between fat and high blood pressure is clearly central to this deadly chain, its biological basis long remained unclear. What is it about fat that impacts vascular function and blood pressure control?
Now, a new study demonstrates how thermogenic beige fat—a type of adipose tissue, distinct from white fat, that helps the body burn energy—directly shapes blood pressure control. Building on clinical evidence that people with brown fat have lower odds of hypertension, the researchers created mouse models that cannot form beige fat (the thermogenic fat depot in mice that most closely resembles adult human brown fat) to watch what happens when this tissue is lost. They found that the loss of beige fat increases the sensitivity of blood vessels to one of the most important vasoconstricting hormones (angiotensin II)—and that blocking an enzyme involved in stiffening vessels and disrupting normal signaling can restore healthy vascular function in mice. These results, published in Science (opens in new window), reveal a previously unknown mechanism driving high blood pressure and point toward more precise therapies that target communication between fat and blood vessels.
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