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Category: neuroscience – Page 9

V-STARS pioneers neuroscience at ESA’s Orbital Robotics Lab

As part of the ESA Academy Experiments Programme, Team V-STARS carried out the first experiment with human participants in the Orbital Robotics Lab, investigating how microgravity affects the perception of verticality.

The V-STARS team, a collaboration between Birkbeck, University of London, and the University of Kent (UK), was selected to join the ESA Academy Experiments Programme in February 2025. After obtaining ethical approval from the United Kingdom and authorisation from the ESA Medical Board, the team was permitted to carry out their experiment in the Orbital Robotics Lab (ORL), located at ESTEC, the ESA site in the Netherlands.

The campaign involved test subjects seated on the ORL’s floating platform, wearing VR headsets while performing gravity-related perceptual tasks. The project investigates the use of Vestibular Stochastic Resonance — a phenomenon in which controlled noise enhances the sensitivity of a sensory system — to improve perception and potentially accelerate adaptation to microgravity. Over two weeks, the team tested more than 20 participants and has now returned to their universities to analyse the results.

Video NeuroImage: Stereotypic Motor Behaviors in a Patient With Pantothenate Kinase–Associated Neurodegeneration

A 24-year-old woman with pantothenate kinase–associated neurodegeneration (PKAN) presented with a 5-year history of psychiatric symptoms followed by prominent stereotypic motor behaviors, including repetitive touching of her mouth and leg, object manipulation, and tip-toe walking (Video 1). Examination revealed severe depression and anxiety, mild speech dysfluency, and the stereotypic movements. Previous symptomatic treatments provided limited benefit. Brain magnetic resonance imaging demonstrated the pathognomonic “eye-of-the-tiger” sign, indicative of iron deposition in the bilateral globus pallidus (Figure). Genetic testing identified compound heterozygous variants in the PANK2 gene: a known pathogenic variant (c.401AG) and a novel likely pathogenic variant (c.1465CG).

A Review of the Clinical Progress of CT1812, a Novel Sigma-2 Receptor Antagonist for the Treatment of Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disease marked by the accumulation of toxic amyloid-beta (Aβ) oligomers. These oligomers are thought to cause synaptic dysfunction and contribute to neurodegeneration. CT1812 is a small-molecule sigma-2 receptor antagonist that is currently being investigated and tested as a potential disease-modifying treatment for AD. CT1812 acts by displacing Aβ oligomers into the cerebrospinal fluid and preventing their interaction with receptors on neurons. Preclinical studies and early clinical trials of CT1812 show promising results and provide evidence for its potential to slow AD progression. This review outlines the role of Aβ oligomers in AD, CT1812’s mechanism of action, and the effectiveness and limitations of CT1812 based on preclinical and clinical studies.

Lab-grown neural circuits reveal thalamus’s key role in cortex development

A Japanese research team has successfully reproduced the human neural circuit in vitro using multi-region miniature organs known as assembloids, which are derived from induced pluripotent stem (iPS) cells. With this circuit, the team demonstrated that the thalamus plays a crucial role in shaping cell type-specific neural circuits in the human cerebral cortex.

These findings were published in the journal Proceedings of the National Academy of Sciences.

Our brain’s cerebral cortex contains various types of neurons, and effective communication among these neurons and other brain regions is crucial for activating functions like perception and cognition.

Blood–Brain Barrier-Targeting Nanoparticles: Biomaterial Properties and Biomedical Applications in Translational Neuroscience

This case-control study found that adults with schizophrenia had significantly greater frontal cortex serotonin release than healthy controls, and greater release correlated with more severe negative symptoms.

Question Is serotonin release altered in vivo in schizophrenia, and is it associated with negative symptom severity?

Findings In this case-control neuroimaging study that included 54 adults, frontal cortex serotonin release was significantly greater in the 26 people with DSM-5 schizophrenia compared with 28 matched healthy controls. In schizophrenia, greater frontal cortex serotonin release was associated with more severe baseline negative symptoms.

Meaning Findings suggest that serotonergic dysfunction in the pathophysiology of schizophrenia was associated with negative symptoms, identifying the regulation of serotonergic neurotransmission as a potential target to treat negative symptoms.

ANK3 as a Novel Genetic Biomarker for Liafensine in Treatment-Resistant Depression: The ENLIGHTEN Randomized Clinical Trial

Liafensine was efficacious and well tolerated in ANK3-positive patients with treatment-resistant depression, with clinically meaningful and statistically significant improvements over placebo, highlighting ANK3 as a predictive genetic biomarker for liafensine.

Question Does the newly discovered ANK3 pharmacogenomic biomarker predict the response of patients with treatment-resistant depression (TRD) to liafensine, a triple reuptake inhibitor, despite failure in a non–biomarker-selected TRD patient population in prior phase 2b trials?

Findings In this randomized clinical trial including 189 ANK3-positive patients with TRD, liafensine demonstrated a 4.4-point Montgomery-Åsberg Depression Rating Scale improvement over placebo, a clinically meaningful and statistically significant difference.

Meaning This represents a first successful genetic biomarker-guided clinical trial in psychiatry, advancing a new treatment for TRD and providing a new path for developing precision medicines in the field.

Ultra‐refractory epilepsy: The newly described entity

“Ultra-refractory epilepsy (URE) is a newly described form of extremely difficult-to-treat epilepsy. In our study of 62 patients, all had already failed at least six different treatment attempts, including medications, brain surgery, or nerve stimulation. Most patients continued to have frequent seizures despite all available therapies, and only a small minority achieved long-term seizure freedom. These findings show that URE is a severe condition with a major unmet medical need, highlighting the importance of developing new treatment strategies.”

Read this original article from Epilepsia Open Journal at doi.org/10.1002/epi4.70196.

Objective Drug-resistant epilepsy (DRE) is defined as the failure of two antiseizure medications (ASMs) to achieve complete seizure control, affecting approximately 30% of epilepsy patients. In some cases, additional ASMs and surgical approaches are also unsuccessful. Ultra-Refractory Epilepsy (URE) is a newly described entity, characterized by the failure of six distinct epilepsy treatment strategies, including ASMs, surgical resection, and neurostimulation techniques. This study aimed to analyze demographic and clinical data of URE patients managed at the Brno Epilepsy Center, a member of the European Reference Network (ERN)—EpiCARE.

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