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.

Summary: A new study finds that long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with a lower risk of developing dementia. Researchers followed 11,745 adults over 14.5 years and found that those who used NSAIDs long-term had a 12% reduced dementia risk.

However, short-and intermediate-term NSAID use did not provide the same benefit, nor was the total cumulative dose linked to risk reduction. These findings suggest that sustained anti-inflammatory effects may play a role in protecting against dementia.

Past neuroscience studies suggest that memories of events that occurred at short time intervals from one another are often connected, via a process referred to as memory linking. While memory linking is now a well-documented phenomenon, its neural underpinnings have not been fully elucidated.

Researchers at the University of California Los Angeles (UCLA) recently carried out a study aimed at better understanding the neural processes that contribute to memory linking in the mouse brain. Their findings, published in Nature Neuroscience, suggest that dendritic plasticity, the adaptation of dendrites (i.e., branch-like extensions of neurons) over time, plays a key role in the linking of memories.

“A few years back, in a landmark study published in Nature in 2016, we demonstrated that memories formed a few hours apart are linked because they are stored in a common set of neurons in the hippocampus,” Alcino Silva, senior author of the paper, told Medical Xpress. “We wanted to know: Where within these neurons are these memories stored and linked? What was causing these neurons to be recruited?”