To mimic the conditions of the human brain, the researchers opted not to use a mouse model for MS, instead advancing a model that uses the marmoset, a nonhuman primate. Compared to mouse brains, marmoset and human brains have a higher ratio of white matter (the “wires” of the brain) to gray matter (neuronal cell bodies). The marmoset model creates multiple lesions that closely resemble those seen in human MS and that can be tracked in real time using MRI imaging. Because these lesions can be induced experimentally, the model offers a look at the earliest stages of inflammation and immune responses that lead to MS-like demyelination.

One key player identified was a specific type of astrocyte, one of the support cell types in the brain, that turns on a gene called SERPINE1 or plasminogen activator inhibitor-1 (PAI1). They found SERPINE1-expressing astrocytes in vulnerable brain borders before visible damage occurs, clustering near blood vessels and the fluid-filled ventricles of the brain and signaling future areas of lesion development. These astrocytes also appeared to influence the behavior of other cells near the lesion area, including the ability of immune cells to enter the brain and contribute to inflammation, as well as the precursor cells involved in myelin repair.

Given that SERPINE1-expressing astrocytes accumulated at the edges of growing lesions, where damage happens but healing also begins, their potential dual role in coordinating signals that could lead to either tissue repair or further damage was an unexpected wrinkle that will require further study. It’s possible that the earliest responses could be a part of a protective mechanism that becomes overwhelmed as the injury progresses. It’s also possible that the same mechanism could itself become disease-causing.

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Using an animal model of multiple sclerosis (MS), researchers have created a four-dimensional brain map that reveals how lesions similar to those seen in human MS form. These findings, published in Science, provide a window into the early disease state and could help identify potential targets for MS treatments and brain tissue repair.

The researchers combined repeated MRI imaging with brain-tissue analysis, including gene expression, to track the onset and development of MS-like lesions. They uncovered a new MRI signature that can help detect brain regions at risk for damage weeks before any visible lesions occur. They also identified “microenvironments” within affected brain tissue based on observed patterns of neural function, inflammation, immune and support cell responses, gene expression, and levels of damage and repair.

“Identifying the early events that occur after inflammation and teasing apart which are reparative versus which are damaging, can potentially help us identify MS disease activity sooner and develop treatments to slow or stop its progression,” said the author.

The brain’s ability to process information is known to be supported by intricate connections between different neuron populations. A key objective of neuroscience research has been to delineate the processes via which these connections influence information processing.

Researchers at the University of Padova, the Max Planck Institute for the Physics of Complex Systems and École Polytechnique Fédérale de Lausanne recently carried out a study aimed at better understanding the contribution of excitatory and inhibitory neuron populations to the brain’s encoding of information. Their findings, published in Physical Review Letters, show that information processing is maximized when the activity of excitatory and inhibitory neurons is balanced.

“Our research was inspired by a fundamental question in neuroscience: how does the structure of the brain shape its ability to process information?” Giacomo Barzon, co-author of the paper, told Medical Xpress. “The brain continuously receives and integrates sensory inputs, and neurons do not act in isolation—they are part of complex, recurrent networks. One particularly intriguing feature of these networks is the balance between the activity of excitatory and inhibitory neurons, which has been observed across different brain regions.”

Radiologically, Chiari malformation type I (CM-I) is characterized by cerebellar tonsil herniation of at least 5 mm through the foramen magnum. In symptomatic cases, posterior fossa decompression (PFD) surgery is often performed and improves symptoms in approximately 75% of patients. However, the surgery involves risks, and identifying which candidates will benefit from surgery is important. It has previously been shown that the amount of tonsillar descent does not correlate with symptom severity or surgical outcomes. The authors hypothesized that using advanced neuroimaging methods to directly measure CSF flow and brain motion will give insights regarding which patients have the greatest likelihood of cerebral dynamic improvements from surgery.

Here, the authors evaluated 108 CM-I patients (age 19–70 years), 61 of whom underwent PFD surgery. The authors used phase-contrast MRI to measure CSF flow/stroke volume and cine displacement encoding with stimulated echoes (DENSE) imaging to measure brain motion, with a goal to predict postsurgical cerebral dynamic improvements from presurgical images.

The authors found that CSF stroke volume increased after PFD surgery by 28.9% (p = 0.014), brainstem motion decreased after surgery by 17.3% (p = 0.002), and cerebellum motion decreased 45.2% (p < 0.001). Notably, the amount of CSF flow increase after surgery had no relationship to tonsillar descent (R = 0.059, p = 0.767) but did relate to the amount of presurgical CSF flow (R = −0.518, p = 0.005). Likewise, improvements to brain motion were better predicted by the amount of presurgical motion (brainstem, R = −0.638, p < 0.001; cerebellum, R = −0.878, p < 0.001) than by tonsillar descent (brainstem, R = −0.312, p = 0.093; cerebellum, R = −0.620, p < 0.001).

A new study suggests a nasal spray developed to target neuroinflammation could one day be an effective treatment for traumatic brain injury (TBI). By studying the effects of the nasal anti-CD3 in a mouse model of TBI, researchers found the spray could reduce damage to the central nervous system and behavioral deficits, suggesting a potential therapeutic approach for TBI and other acute forms of brain injury. The results are published in Nature Neuroscience.

The study examines the monoclonal antibody Foralumab, made by Tiziana, which has been tested in clinical trials for patients with multiple sclerosis, Alzheimer’s disease, and other conditions.

Multiple experiments were done in mouse models with moderate-to-severe traumatic brain injury to explore the communication between regulatory cells induced by the nasal treatment and the microglial immune cells in the brain. Over time, researchers were able to identify how they modulate immune response.

In addition to assessing the effects of the treatment, the research team was able to learn about immune response over time and compare the immune responses and effects of TBI in the mice.

The next step in the research is to translate the findings from preclinical models to human patients.

Scientists have identified the 1N4R tau isoform as a key driver of Alzheimer’s.

Alzheimer’s disease is a progressive neurological disorder that primarily affects older adults, leading to memory loss, cognitive decline, and behavioral changes. It is the most common cause of dementia. The disease is characterized by the buildup of amyloid plaques and tau tangles in the brain, which disrupt cell function and communication. There is currently no cure, and treatments focus on managing symptoms and improving quality of life.