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Category: neuroscience

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.

Brain ‘Zaps’ From Contact Lenses May Help Ease Depression, Mouse Study Shows

Scientists in South Korea have developed experimental contact lenses designed to send electrical signals through the retina and into brain regions linked to mood. In mice, the technology appeared to improve depression-like behaviour.

The idea sounds futuristic: a contact lens that could one day help treat depression by stimulating the brain through the eye. The work is still at a very early stage, with findings so far limited to a single mouse study.

The eye is already one of the body’s most useful access points for medical technology.

This Gene Is Linked to Lower Alzheimer’s Risk — And We May Finally Know Why

There’s something special about the APOE2 variant of the APOE (apolipoprotein E) gene: People who carry it tend to live longer, and they have a lower risk of developing Alzheimer’s disease.

Scientists are still trying to figure out why, and now, they have a new lead.

A team led by researchers at the Buck Institute for Research on Aging in the US set out to answer that question using human stem cell-derived neurons and mouse studies.

A new imaging approach captures brain activity across nine cell types at once

Scientists at the Max Planck Florida Institute for Neuroscience (MPFI), in collaboration with ZEISS and MetaCell, have developed a powerful new imaging pipeline called Neuroplex. As described in a paper published in eLife, the technique allows simultaneous monitoring of the activity of up to nine distinct neuronal populations in freely moving mice, dramatically accelerating the pace of scientific exploration into how the brain controls behavior.

For years, neuroscientists linking brain activity to behavior have faced a fundamental limitation: Miniscopes, the tiny head-mounted microscopes used to observe neural activity in behaving animals, could capture neural activity, but couldn’t reliably distinguish more than two different types of brain cells at a time.

“To understand the brain, we need to link patterns of activity in specific neurons to behavior,” stated lead author Dr. Mary Phillips. “We can readily use labels to color-code different populations of neurons, but when using miniscopes to correlate neural activity to behavior, we couldn’t distinguish more than two of these populations. This made it difficult to compare the activity across multiple cell types and circuits to understand how specific circuits regulate behavior.”

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