New 2025 studies show human milk oligosaccharides may support gut, immune, metabolic, and brain health in adults. Here is what the science reveals.
Category: neuroscience – Page 5
The ‘silent’ brain cells that shape our behaviour, memory and health
Researchers peered through microscopes, hooked up electrodes, and built entire careers around one cell type: neurons. These electrically active cells were clearly the brain’s protagonists, zipping signals through our heads at lightning speed to create thoughts, memories, and movements. Everything else—especially the star-shaped cells called astrocytes that outnumber neurons—was dismissed as mere scaffolding. Glial cells, they were called: “glue.”
Inbal Goshen, a memory researcher at Hebrew University of Jerusalem, remembers feeling like an outsider when she started investigating astrocytes in the early 2010s. “Oh, that’s the weird one who works on astrocytes,” she imagined colleagues whispering at conferences. The skepticism was palpable. Yet new molecular tools had finally given her a way to peek into these mysterious cells, and what she found was too intriguing to ignore.
Unlike neurons, astrocytes don’t fire electrical signals. They were “electrically silent,” which is why they’d been ignored. But they were whispering in another language entirely: calcium. Using advanced imaging, researchers discovered that astrocytes communicate through slow, rhythmic waves of calcium signals—more like a gentle tide than neuron’s lightning strike. And their reach is astonishing: a single human astrocyte can touch up to two million synapses, the junctions where neurons meet. Their bushy tendrils fill every crevice of the brain, each cell nestling against neurons and blood vessels, creating an intimate, three-way relationship.
Memory research revealed another layer. Goshen’s team watched astrocytes in mice navigating toward water rewards. As the animals approached familiar prize locations, astrocyte activity slowly ramped up—but showed no response in new environments. The cells were encoding spatial memories, not just supporting them. Other labs found that astrocytes help stabilize and recall fear memories, their slow calcium signals perfectly suited to bridge the gap between learning something and remembering it days later. As neuroscientist Jun Nagai describes it, “Think of them as the brain’s long-exposure camera: they capture the trace of meaningful events that might otherwise fade too fast.”
Astrocytes make up one-quarter of the brain, but researchers are only now realizing their true value.
Adolescence lasts into 30s, new study shows | BBC News
The brain goes through five distinct phases in life, with key turning points at ages nine, 32, 66 and 83, scientists have revealed.
Around 4,000 people up to the age of 90 had scans to reveal the connections between their brain cells.
Researchers at the University of Cambridge showed that the brain stays in the adolescent phase until our early thirties when we \.
Scientists discover first gene proven to directly cause mental illness
Scientists have discovered that a single gene, GRIN2A, can directly cause mental illness—something previously thought to stem only from many genes acting together. People with certain variants of this gene often develop psychiatric symptoms much earlier than expected, sometimes in childhood instead of adulthood. Even more surprising, some individuals show only mental health symptoms, without the seizures or learning problems usually linked to GRIN2A.
Abstract: 1 Institut de Neurociències, and
1 Institut de Neurociències, and.
2Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Bellaterra, Barcelona Spain.
3Institute of Neuroscience, CSIC-UMH, Alicante, Spain.
4Neurodegenerative Diseases Research Group, Vall d’Hebron Research Institute-Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Barcelona, Spain.
How the brain protects itself from Alzheimer’s disease
High levels of calcium are toxic to cells and contribute to loss of neurons in Alzheimer’s disease. A new study published in JCI Insight identifies a mechanism through which the young brain protects itself against high calcium levels, and it could help scientists learn how to protect the brain from this devastating neurodegenerative condition.
Glyoxalase 1 (GLO1) is a protein that plays an essential role in getting rid of toxic byproducts in cells. In the study, Yale School of Medicine (YSM) researchers discovered elevated GLO1 levels in the brains of animals with excessive levels of cellular calcium, finding that the brain increased GLO1 expression as a protective mechanism to mitigate the effects of the calcium dysregulation.
However, with advancing age, GLO1 activity declined, the researchers found, which may make the brain less resilient to neurodegeneration. The study could inform the development of therapeutics that target GLO1 and prevent neurodegeneration.
Cracking the code of Parkinson’s: How supercomputers are pointing to new treatments
More than 1 million Americans live with tremors, slowed movement and speech changes caused by Parkinson’s disease—a degenerative and currently incurable condition, according to the Parkinson’s Foundation and the Mayo Clinic. Beyond the emotional toll on patients and families, the disease also exerts a heavy financial burden. In California alone, researchers estimate that Parkinson’s costs the state more than 6 billion dollars in health care expenses and lost productivity.
Scientists have long sought to understand the deeper brain mechanisms driving Parkinson’s symptoms. One long-standing puzzle involved an unusual surge of brain activity known as beta waves—electrical oscillations around 15 Hertz observed in patients’ motor control centers. Now, thanks to supercomputing resources provided by the U.S. National Science Foundation’s ACCESS program, researchers may have finally discovered what causes these waves to spike.
Using ACCESS allocations on the Expanse system at the San Diego Supercomputer Center—part of UC San Diego’s new School of Computing, Information, and Data Sciences—researchers with the Aligning Science Across Parkinson’s (ASAP) Collaborative Research Network modeled how specific brain cells malfunction in Parkinson’s disease. Their findings could pave the way for more targeted treatments.
ALS treatment using RNA-based gene therapy
The current study was based on a feature of ALS discovered previously in the lab: toxic clusters (aggregates) of a protein called TDP-43 (usually responsible for regulating protein production at the site) form at the tip of the nerve, where it meets the muscle. To discover how these TDP-43 aggregates are formed, the researchers used a mouse model for ALS, tissues from ALS patients, and cultures of human stem cells.
The study found that muscle cells produce small RNA molecules called microRNA-126 and send them in vesicles, through the synapsis, to the tip of the nerve cell. The role of these molecules is to prevent the expression of the TDP-43 protein at the neuromuscular junction when it is not needed.
The author explains: “We discovered that in ALS, the muscle produces a smaller amount of microRNA-126, which leads to an excess of TDP-43. The excess protein forms toxic aggregates that attack molecules essential for functioning of the mitochondria — the nerve cell’s powerhouse. Damage to the mitochondria causes an energy deficit, gradually destroying motor neurons and leaving patients’ muscles paralyzed.”
The study further showed that when the amount of microRNA-126 is reduced, a process similar to ALS occurs, and the neurons are destroyed. Conversely, increasing the level of microRNA-126 in tissues taken from ALS patients and in ALS model mice led to a decrease in the levels of TDP-43, and the neurons stopped degenerating and even regenerated.
The researchers concluded that adding microRNA-126 rescues neurons damaged by ALS, prevents degeneration of the neuromuscular junction, and could serve as a basis for developing effective drugs for this currently incurable disease.
Researchers in this study opened a new avenue for treating the fatal degenerative disease ALS, considered incurable until now. The researchers identified a new molecular mechanism that plays a key role in the disease and were able to neutralize it through gene therapy.