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Category: neuroscience – Page 25

Treating age‐related loss of muscle mass and function: Where should we be focusing?

Aging human breast atlas reveals cancer susceptibility

The team used advanced imagining techniques to analyse breast tissue from more than 500 women aged 15 to 86 years old. The tissue included biopsies taken from women for non-cancer-related reasons.

Combining these images with details of the hormone receptors and immune cells present, as well as the tissue architecture, the researchers were able to map how breast tissue changes over time in unprecedented detail. Their findings point to reasons why breast cancer risk increases with age and why tumors in younger women differ biologically.

The author added: “Our map revealed that as women age, their breast tissue goes through major changes, with the most dramatic changes occurring at menopause. There are changes, too, during their twenties, possibly linked to pregnancy and childbirth, but these are far less pronounced.”

The map revealed that all types of cells become fewer in number and divide far less often. Milk-producing structures known as lobules shrink or disappear, while the ducts that that carry milk become relatively more common, with the supporting layer around them becoming thicker. Fat cells increase while blood vessels decrease.

Meanwhile, changes occur in the immune environment. Younger breasts have more B cells and active T cells, which helps them identify and kill cancer cells. As tissue ages, these types of cells decline in number, replaced by other types of immune cell that indicate a more inflammatory and potentially less protective immune environment. ScienceMission sciencenewshighlights.

Continue reading “Treating age‐related loss of muscle mass and function: Where should we be focusing?” | >

Cytokine-armored CAR-T cell therapy helps eliminate aggressive brain tumors in preclinical study

Scientists at the UCLA Health Jonsson Comprehensive Cancer Center have developed a new cytokine-armored CAR-T cell therapy that helps the immune system better attack aggressive brain tumors in mice while reducing dangerous side effects that have long limited immune-based treatments for glioblastoma, one of the deadliest and most treatment-resistant brain cancers.

The therapy works by reprogramming CAR-T cells to release immune-stimulating proteins, called IL-12 and DR-18, that activate the body’s own immune system, strengthening the overall anti-cancer response. In mouse models, the approach improved tumor control, including against cancers made up of mixed cell populations that often escape therapies.

Researchers also found that pairing the treatment with a second CAR-T strategy targeting VEGF, a protein that drives abnormal blood vessel growth and contributes to swelling in glioblastoma, helped reduce side effects while preserving strong anti-tumor activity.

Scientists may have found the brain’s switch for chronic pain

Scientists may have found the brain’s “pain switch”—and how to turn it off. New research from the University of Colorado Boulder points to a little-known brain circuit that may determine whether short-term pain fades away or becomes a long-lasting problem. The findings suggest that this pathway plays a key role in turning temporary pain into chronic pain that can persist for months or even years.

The study, conducted in animals and published in the Journal of Neuroscience, focused on a region called the caudal granular insular cortex (CGIC). Researchers found that shutting down this circuit can both prevent chronic pain from developing and stop it after it has already begun.

“Our paper used a variety of state-of-the art methods to define the specific brain circuit crucial for deciding for pain to become chronic and telling the spinal cord to carry out this instruction,” said senior author Linda Watkins, distinguished professor of behavioral neuroscience in the College of Arts and Sciences. “If this crucial decision maker is silenced, chronic pain does not occur. If it is already ongoing, chronic pain melts away.”

Glucose nanoparticles help CBD cross the blood-brain barrier

Breakthrough in brain medicine: a new way to deliver CBD!

Cannabidiol (CBD) has incredible potential to fight brain inflammation, but it has always faced a major roadblock: it struggles to dissolve and cross the blood-brain barrier. Researchers have just developed an ingenious solution using glucose-coated nanoparticles to get CBD exactly where it needs to go.

Here’s why it’s a game-changer: 🔬 Sneaky Delivery: The glucose coating helps the particles “hitch a ride” on the brain’s natural glucose transporters, successfully smuggling the CBD across the blood-brain barrier. 🎯 Smart Release: Once inside the brain, the nanoparticles target immune cells (microglia) and only release the CBD when they detect the chemical stress of active inflammation. 🐁 Promising Results: In mouse models of Parkinson’s disease and depression, this new delivery method drastically reduced inflammation, protected neurons, and improved behavioral recovery compared to standard CBD.

This targeted approach could be a massive step forward in treating chronic neuroinflammatory diseases! 🧬✨

Studty.

Glucose-coated nanoparticles carry CBD across the blood-brain barrier, trigger release in inflamed tissue, and reduce neuroinflammatory signs in mice.

Continue reading “Glucose nanoparticles help CBD cross the blood-brain barrier” | >

Biomimetic Microfibers for Myelin-Enhancer Screening and Neural Regeneration

Roles of lysosomal small-molecule transporters in metabolism and signaling

Small-molecule transporters of the lysosomal membrane export lysosomal catabolites for reuse in cell metabolism.

These transporters often show substrate promiscuity and, conversely, a given metabolite is often exported through distinct transport routes and sometimes in different states (e.g., single amino acids versus dipeptides).

Some lysosomal transporters import metabolites into the lumen. The combination of importers and exporters can create small-molecule shuttles across the lysosomal membrane, which regulate the lumen state.

Some lysosomal transporters participate in intracellular signaling cascades. sciencenewshighlights ScienceMission https://www.cell.com/trends/cell-biology/fulltext/S0962-8924(25)00222-3 https://sciencemission.com/lysosomal-small-molecule-transporters

Remyelination requires the precise wrapping of axons by oligodendrocyte processes, a critical step for restoring neural circuit function. However, a lack of quantitative systems that recapitulate axonal geometry and chemistry has limited mechanistic and pharmacological insights into myelin wrapping. Here, we present a bioengineered microfiber platform that mimics neurite architecture and surface chemistry, enabling high-content quantification of oligodendrocyte wrapping. Through compound screening, we identified dimemorfan, a clinically used sigma-1 receptor agonist, as a potent enhancer of myelin wrapping. Dimemorfan treatment accelerated remyelination and functional recovery in demyelinated mice and promoted myelin wrapping by human induced pluripotent stem cell (iPSC)-derived oligodendrocytes.

Continue reading “Biomimetic Microfibers for Myelin-Enhancer Screening and Neural Regeneration” | >

Neutrophils manufacture schizophrenia-linked protein, according to new research

The most common white blood cells in your body—immune cells called neutrophils—can make a protein nobody knew they were making, Stanford Medicine investigators have discovered. That unexpected sighting joins a growing list of hints tying schizophrenia, a disorder of the brain, to events occurring elsewhere in our bodies. The findings are summarized in a paper published in Proceedings of the National Academy of Science.

The newly noticed neutrophil nexus, as a source of the protein called C4A, links a long list of other observations that are somewhat puzzling when looked at in isolation: For example, large-scale population-genetic studies have identified C4A, already known to be produced mainly in the liver, as a pronounced risk factor in schizophrenia. People with schizophrenia tend to have increased numbers of neutrophils in their blood. And the most effective medication for schizophrenia inhibits neutrophils.

Schizophrenia affects one in every 100 persons globally almost without variation by geography or ethnicity. Its most noticeable symptoms are hallucinations, delusions and fixations. A fundamental feature of the disease is cognitive impairment: inability to think clearly, reduced working memory, disorganized thinking and behavior.

Pronounced Neuroplasticity in the Primary Visual Cortex of the Thirteen-lined Ground Squirrel During Hibernation

Hibernating animals can show neuroplasticity throughout the hibernation season. In ground squirrels, decreased dendritic arborization in the hippocampus, somatosensory cortex, and thalamus during deep hibernation (“torpor”) suggests that this neuroplasticity is a brain-wide phenomenon. However, the degree to which neuroplasticity occurs in the visual system is not clear. While transient retinal changes have been reported during torpor, neuroplasticity beyond the retina remains unknown. Here, we characterized hibernation-related neuroplasticity in the primary visual cortex (V1), the first cortical area to receive visual information, in the thirteen-lined ground squirrel (Ictidomys tridecemlineatus). We compared neuronal morphology in Golgi-stained samples from male and female hibernating or non-hibernating squirrels. For the hibernating squirrels, brain tissue was sampled during two different epochs: torpor and inter-torpor arousal. Dendritic arborization decreased during torpor in V1 layer 2/3 pyramidal neurons, manifesting as decreases in dendritic length, number, and complexity. These changes fully reversed during inter-torpor arousal, indicating that on average dendritic arbors grew by 0.75 mm (65%) over ∼1.5 hours. No morphological differences between hibernating and non-hibernating squirrels were apparent when compared 6 months after the hibernation season. We also found no neuroplastic changes in V1 layer 4 spiny stellate neurons, unlike in this cell type the somatosensory cortex. Together, this revealed, for the first time, hibernation-related neuroplasticity in V1 in support of a brain-wide mechanism but with area-specific differences. The speed and magnitude of this naturally occurring neuroplasticity could make ground squirrel V1 a powerful translational model system for conditions requiring neuroplasticity, such as recovery from stroke.

Significance Statement This study is the first demonstration of pronounced hibernation-related neuroplasticity in the primary visual cortex of ground squirrels. Layer 2/3 pyramidal neurons in the primary visual cortex (V1) reduced arborization during torpor. Within 1.5 hours after arousal from torpor, the arborization reversed to non-hibernation levels. The extent and speed of this naturally occurring neuroplasticity could make the relatively well-understood V1 of ground squirrels a powerful translational model system. Complementing insights on neuroplasticity in V1 during development, it has the potential to be leveraged for the study of treatment mechanisms and conditions requiring neuroplasticity, ranging from neurodegeneration to recovery after stroke.

Your Eyes Could Reveal Your Risk of Osteoporosis, Study Finds

The eyes are a window into our deeper health.

As the only outward extension of the central nervous system, these sensory organs may reflect not only the state of our brain and blood vessels, but also our very bones.

Population studies in Singapore and the UK have now revealed that a person’s risk of osteoporosis may be associated with how quickly their eyes are aging.

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