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Category: neuroscience – Page 2

Persistent Hemiplegic Migraine in a Child With CACNA1A Sequence Variation and New-Onset Cerebellar Atrophy: A Pediatric Stroke Mimic

Imaging results also demonstrated marked cerebellar atrophy, which is a recognized feature of CACNA1A-related disorders.13 Although the timing and progression of this abnormality are uncertain because UL last underwent brain imaging in infancy, the need for structured evaluation throughout development is clear. We also noted asymmetric fluid-attenuated inversion recovery signal in the left mesial temporal lobe, which was believed to be most consistent with postictal edema given the known overlap between CACNA1A channelopathies and seizure susceptibility.

This case highlights the diagnostic uncertainty of CACNA1A-related hemiplegic migraine and emphasizes the need for early exclusion of stroke and seizure, in addition to timely escalation of preventive therapy when symptoms persist beyond their typical timeframes. The clinical response to an increased acetazolamide dose, initiation of verapamil, and corticosteroids for cerebral edema provides additional support for current recommendations in a field where high-quality evidence remains limited.

MRI antenna can boost image quality and shorten scan times—without changing existing machines

Magnetic resonance imaging (MRI) is one of medicine’s most powerful diagnostic tools. But certain tissues deep inside the body—including brain regions and delicate structures of the eye and orbit that are of particular relevance for ophthalmology—are difficult to image clearly. The problem is not the scanner itself, but the hardware that sends and receives radio signals.

Now, researchers led by Nandita Saha, a doctoral student in the Experimental Ultrahigh Field Magnetic Resonance lab of Professor Thoralf Niendorf at the Max Delbrück Center have developed an advanced materials-based MRI antenna that overcomes these limitations—delivering enhanced images more quickly and that can be used in existing MRI machines. The research was published in Advanced Materials.

Niendorf and his team worked closely with researchers at Rostock University Medical Center, combining expertise in MRI physics with clinical ophthalmology and translational imaging. The Rostock team is also supporting clinical validation of the technology.

Emerging mechanisms of psilocybin-induced neuroplasticity

Psilocybin, a serotonergic psychedelic, is gaining attention for its rapid and sustained therapeutic effects in depression and other hard-to-treat neuropsychiatric conditions, potentially through its capacity to enhance neuronal plasticity. While its neuroplastic and therapeutic effects are commonly attributed to serotonin 2A (5-HT2A) receptor activation, emerging evidence reveals a more nuanced pharmacological profile involving multiple serotonin receptor subtypes and nonserotonergic targets such as TrkB. This review integrates current findings on the molecular interactome of psilocin (psilocybin active metabolite), emphasizing receptor selectivity, biased agonism, and intracellular receptor localization.

Astrocytes, not just neurons, found to drive fear memory signals in the amygdala

Picture a star-shaped cell in the brain, stretching its spindly arms out to cradle the neurons around it. That’s an astrocyte, and for a long time, scientists thought its job was caretaking the brain, gluing together neurons, and maintaining neural circuits. But now, a new study reveals that these supposed support cells that are spread all over the brain are as important as neurons in fear memory.

“Astrocytes are interwoven among neurons in the brain, and it seemed unlikely they were there just for housekeeping. We wanted to understand what they’re actually doing—and how they’re shaping neural activity in the process,” said Lindsay Halladay, assistant professor at the University of Arizona Department of Neuroscience and one of the study’s senior authors.

Halladay’s lab collaborated with researchers from the National Institutes of Health for this multi-institutional study, led by Andrew Holmes and Olena Bukalo of the Laboratory of Behavioral and Genomic Neuroscience.

Five Years of Ublituximab in Multiple Sclerosis: ULTIMATE I and II Open-Label Extension Study

Five years of ublituximab treatment in MultipleSclerosis demonstrated sustained reduction in relapse rates and confirmed disability progression, with safety profile consistent over time.

Question What is the long-term clinical efficacy and safety of ublituximab in people with relapsing multiple sclerosis (RMS)?

Findings In this trial including 985 adults, participants treated with continuous ublituximab for up to 5 years in the open-label extension study after completion of the randomized Study to Assess the Efficacy and Safety of Ublituximab in Participants With Relapsing Forms of Multiple Sclerosis (ULTIMATE) had significantly lower annualized relapse rate and confirmed disability progression than those initially treated with teriflunomide. The overall safety profile of ublituximab remained consistent with no new safety signals emerging with prolonged treatment.

Meaning Results suggest that early initiation of ublituximab and continued treatment over a period of 5 years provided sustained clinical benefits in participants with RMS.

Polyamine metabolism as a regulator of cellular and organismal aging

Polyamines — putrescine, spermidine, and spermine — are ubiquitous cationic molecules that are essential for cellular proliferation and homeostasis. Their intracellular concentrations decline with age, contributing to physiological and cognitive deterioration. Recent studies have revealed that spermidine supplementation extends lifespan and improves cognitive and cardiac function in various model organisms, suggesting that maintaining polyamine balance has anti-aging potential. Polyamine metabolism is tightly regulated through biosynthesis, degradation, and transport; however, age-associated upregulation of spermine oxidase (SMOX) and accumulation of its toxic byproduct acrolein promote oxidative damage and cellular senescence. Suppressing SMOX activity or polyamine degradation attenuates senescence markers and DNA damage, highlighting spermine catabolism as a therapeutic target. Polyamines also modulate epigenetic regulation, including DNA methylation and histone acetylation, thereby influencing gene expression and chromatin structure during aging. Moreover, polyamine-dependent hypusination of eIF5A sustains protein synthesis in senescent cells. These multifaceted actions indicate that polyamine metabolism integrates redox control, translational regulation, epigenetic maintenance and autophagy to determine cellular and organismal longevity. While animal studies demonstrate clear anti-aging effects of spermidine and spermine, human clinical evidence remains limited, with variable outcomes likely due to bioavailability and metabolic conversion. Future strategies combining dietary or probiotic polyamine enhancement, enzyme-targeted inhibitors, and personalized metabolic interventions hold promise for extending healthspan. Collectively, maintaining optimal polyamine homeostasis emerges as a key approach to counteract aging and age-related diseases.

Role of Dopamine in Pain

Dopamine is a member of a class of molecules called the catecholamines, which serve as neurotransmitters and hormones. In the brain, dopamine serves as a neurotransmitter and is released from nerve cells to send signals to other nerves. Outside of the nervous system, it acts as a local chemical messenger in several parts of the body.

Image Copyright: Meletios, Image ID: 71,648,629 via shutterstock.com

A number of important neurodegenerative diseases are associated with abnormal function of the dopamine system and some of the main medications used to treat those illnesses work by changing the effects of dopamine. The condition Parkinson’s disease is caused by a loss of dopamine secreting cells in a brain area called the substantia nigra.

Grant supports research into how microglia may spread toxic tau in Alzheimer’s

A paper describing Hopp’s upcoming study published on the CureAlz website, titled, “How Do Microglia Contribute to the Spread of Tau Pathology in Alzheimer’s Disease?”, says that while tau aggregates are a defining feature of Alzheimer’s disease and closely track with brain cell loss, memory problems and cognitive decline, much still isn’t known about how it spreads or what role the brain’s immune system plays in the process.

There is evidence, it says, that toxic forms of tau, which have become “misfolded” or dysfunctional, act like a “bad influence.”

“When they encounter nearby healthy tau proteins, they cause them to misfold as well, triggering a chain reaction that spreads from one brain region to another,” according to the paper. “Microglia … are among the first to encounter these toxic tau ‘seeds.’ Normally, microglia protect the brain by clearing debris and helping repair damage. But growing evidence suggests that microglia may also contribute to tau’s spread by engulfing misfolded tau and inadvertently releasing it, thereby amplifying its harmful effects.”

A researcher with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio has received a two-year, $402,500 grant award from the Cure Alzheimer’s Fund to study how microglia, the brain’s resident immune cells, paradoxically might contribute to the spread of toxic forms of tau protein in the disease.

Sarah C. Hopp, PhD, associate professor of pharmacology with the Biggs Institute and the South Texas Alzheimer’s Disease Research Center, along with her lab have been instrumental in uncovering the behavior of microglia. UT Health San Antonio is the academic health center of The University of Texas at San Antonio.

Starting this month, Hopp’s lab will test the hypothesis that microglial uptake of tau is a key mechanism driving its spread through the brain, and that specific molecular pathways determine whether this process protects or harms neurons. The Cure Alzheimer’s Fund, also known as CureAlz, is a nonprofit organization that funds research “with the highest probability of preventing, slowing or reversing Alzheimer’s disease.”

Continue reading “Grant supports research into how microglia may spread toxic tau in Alzheimer’s” | >

Key alterations discovered in the cerebral cortex of people with psychosis

Researchers at the University of Seville have analyzed alterations in the cerebral cortex in people suffering from psychosis. Their findings show that psychosis does not follow a single trajectory, but rather its evolution depends on a complex interaction between brain development, symptoms, cognition and treatment. The authors therefore emphasize the need to adopt more personalized approaches that take individual differences into account in order to better understand the disease and optimize long-term therapeutic strategies.

Psychosis is a set of symptoms—such as hallucinations and delusions—that are common in schizophrenia and involve a loss of contact with reality. From their first manifestation, known as the first psychotic episode, these symptoms can appear and evolve in very different ways between individuals, thus making schizophrenia a particularly complex disorder.

The results of the study show that, at the time of the first episode, people with psychosis present a reduction in cortical volume, which is particularly marked in regions with a high density of serotonin and dopamine receptors, key neurotransmitters in both the pathophysiology of psychosis and the mechanism of action of antipsychotics. The data also suggest that both neurons and other brain cells involved in inflammatory and immunological processes may play an important role in the disease.

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