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The appropriate acute treatment strategy for minor ischemic stroke, defined as National Institutes of Health Stroke Scale scores $$5, is not as well-defined. Prior studies have demonstrated mixed results regarding the effects of neurovascular interventions on minor stroke patients for optimizing the chances of symptomatic improvement. We performed a retrospective single-center study across 6 years to determine the association between thrombolytics and the likelihood of clinical symptom improvement by 24 h in minor stroke patients across ages. Margin plots were derived from multivariable regression analyses. Of 1172 minor stroke patients, in patients <70 years of age, there was greater than 50% likelihood of improvement with any type of thrombolytic administration. When substratifying by type of thrombolytic, there is greater than 50% odds of improvement in patients <80 years of age treated with alteplase and <70 years of age treated with tenecteplase. Thus, the association between age and likelihood of benefit after thrombolytic treatment in minor stroke patients highlights particular minor stroke subpopulations, particularly younger patients, who may benefit from thrombolytic treatment.

Myasthenia gravis (MG) is an autoimmune disorder driven by pathogenic IgG autoantibodies, leading to muscle weakness and impaired quality of life. Conventional immunosuppressant therapies are often limited by side effects and incomplete efficacy. Nipocalimab-aahu (N-a), recently FDA-approved, is a novel neonatal Fc receptor (FcRn) antagonist that reduces circulating IgG levels, targeting the underlying disease mechanism. This review synthesizes evidence on N-a's efficacy, safety, and clinical positioning. Phase 2 and 3 trials (Vivacity-MG/MG3) demonstrated that N-a significantly improves the Myasthenia Gravis Activities of Daily Living (MG-ADL) score compared to placebo, with a favorable safety profile. The most common adverse events were nasopharyngitis and headache, with no increased serious infection risk or clinically significant hypoalbuminemia. Compared to other biologics, N-a offers a distinct mechanism, selective IgG reduction without broad immunosuppression and a convenient bi-weekly dosing regimen. While it shows promise for reduced systemic immunosuppression and potentially greater efficacy in MG-ADL improvement than some alternatives, cross-trial comparisons are limited. Key limitations include the need for long-term safety data and more research in underrepresented populations, including pediatric and seronegative patients. In conclusion, N-a represents a significant advancement in generalized MG (gMG) treatment, providing a targeted, effective, and well-tolerated option that addresses a key unmet need for patients with acetylcholine receptor (AChR) or muscle-specific kinase (MuSK) antibody-positive disease.

Synaptic adhesion molecules (SAMs) are glycoproteins localized on neuronal surfaces, primarily expressed at synaptic plasma membranes. SAMs play a role in inducing formation, maturation, plasticity, and assembly of synaptic connections, which are vital for normal neurodevelopment. SAMs link the pre- and post-synaptic compartments and assist in inter-synaptic signaling and recognition. An increasing variety of SAMs, including neurexins and neuroligins, immunoglobulin (Ig) domain proteins-like synaptic cell adhesion molecule (SynCAM) and neural cell adhesion molecule, receptor phosphotyrosine kinases and phosphatases, as well as various leucine-rich repeat proteins, have been identified. Neurodevelopmental disorders (NDDs), like autism, attention deficit hyperactivity disorder, intellectual disabilities, and cerebral palsy, have been associated with altered SAMs. NDDs are characterized by a spectrum of challenges stemming from abnormal brain development. The etiology of these disorders involves the interaction between genes and environmental factors, such as metals. This review aims to provide a comprehensive overview of the literature, highlighting the role of SAMs in NDDs and potential mechanisms via which neurotoxic metals may contribute to the pathogenesis of NDDs that could involve perturbations in SAMs. Understanding these interconnections will assist in identifying therapeutic targets for these disorders.

The use of iron oxide nanoparticles (IONPs) in magnetic resonance imaging (MRI) and the study of brain functions using MRI have been continuously evolving for more than 30 years. This contribution aims to explore the recent applications of magnetic IONPs in the study of the brain through functional MRI (fMRI), particularly focusing on their use in a specific parameter, that is, the cerebral blood volume (CBV), whose measurements are valued for their higher sensitivity and spatial specificity with respect to blood oxygen level-dependent (BOLD) fMRI analyses. This study will summarize the basis of the fMRI technique, explaining the types of experiments commonly conducted, the parameters involved, and discussing the main techniques that exploit magnetic nanoparticles and other materials as contrast agents, along with their potential applications in the imaging field. CBV measurements will be explained in general theoretical terms and compared with other methods. The key elements of magnetic nanoparticle production, including the most commonly used synthesis procedures and coating options, will be reported. Finally, the discussion will focus on how CBV-weighted (CBVw) images acquired using IONPs are currently being utilized in research.

The evolving research on the interactions between pain and mental disorders underscores the critical role of neuroimmune interplay in shaping pain perception and mental illness progression. This study employs bibliometric analysis to scrutinize the research landscape, identify emerging hotspots, and forecast future directions. A systematic review of literature from 2014 to 2023 was conducted using CiteSpace software for co-citation analysis, keyword co-occurrence, and burst detection to identify research hotspots and trends. The study examined developmental trends in pain and psychiatric disorder research, highlighting major research institutions and key themes. It unveils pivotal contributors and collaborative networks, showing significant growth in recent years. Emphasis is placed on neuroinflammation and neuroimmunomodulation interactions with mental illnesses. Keyword and thematic clustering analyses highlight the roles of microglial activation, inflammatory mediators, neurotransmitters, and emotional regulation processes. This study paves the way for future inquiries into neuroimmune mechanisms, the development of personalized treatment strategies, and an interdisciplinary approach to enrich our understanding of the biopsychosocial model in these conditions. Future studies should delve deeper into the molecular intricacies of these interactions to develop more effective therapeutic strategies, aiming to enhance patients' quality of life.

Depending on the impact of emotions on a person's performance and emotional disorders that can be the main cause of many mental illnesses, as well as the desire of technology to design machines that are able to change their performance according to a person's emotional states, the study of electroencephalography (EEG) signals to analyze the different dimensions of human emotions has become increasingly significant. Based on machine learning models, this study was designed to identify the five emotions of relaxation, happiness, motivation, sadness and fear using EEG signal analysis. EEG data were collected from 23 male master's students at Tabriz University, aged 24–31, as they watched five videos designed to elicit different emotional responses. After preprocessing to remove noise and artifacts, we extracted statistical and frequency-domain features from the raw signal. The features were labeled and selected using statistical tests. In the final step, five different emotions were classified using decision tree, linear discriminant analysis (LDA), Naive Bayes, support vector machine (SVM), K-nearest neighbor (KNN), ensemble, logistic regression and neural network. It has been verified that ensemble and decision tree models had the highest accuracy with 95.38% and 91.77%.

N6-methyladenosine (m6A), the most abundant internal modification in mammalian mRNA, plays a critical role in cognitive function by dynamically regulating gene expression. This narrative review examines m6A's role in cognitive processes and its potential impact on perioperative neurocognitive disorders (PNDs), which encompass a spectrum including postoperative delirium, delayed neurocognitive recovery, and postoperative cognitive dysfunction. The m6A regulatory machinery—comprising methyltransferases (“writers”), demethylases (“erasers”), and recognition proteins (“readers”)—modulates neuronal development, synaptic plasticity, and cognitive processes by influencing mRNA stability, translation, and degradation. Evidence from animal models indicates that m6A dysregulation contributes to neuroinflammation, neurodegeneration, and neuronal injury, which are pathophysiological mechanisms implicated in PNDs. Notably, anesthetic agents and surgical stress have been shown to alter hippocampal m6A levels, and manipulation of m6A-related proteins may ameliorate cognitive deficits. While these findings suggest potential mechanistic connections, direct evidence specifically linking m6A modifications to PNDs pathogenesis remains preliminary and largely based on preclinical models. Further research is needed to establish causal relationships, identify m6A-modified targets relevant to PNDs pathology, and evaluate m6A as a potential biomarker or therapeutic target. This review provides a foundation for understanding how m6A modification may influence perioperative cognitive outcomes and identifies promising avenues for future investigation.

In psychopathology, one of the most complex challenges is offered by the diagnostic comparison between patients with borderline personality disorder and those with bipolar spectrum disorder, as some of the symptoms characterizing the two disorders overlap. This detail can mislead therapists who are often called upon to diagnose these syndromes, and in some cases, there is a tendency to diagnose both as one is a personality disorder and the other is a mood disorder. This article provides the reader with a complete overview of these two disorders, highlighting some aspects that could redefine their clinical framework. This need could favor a reduction in cases of diagnostic error, also through the proposal of an innovative psychometric tool, Perrotta Border-Bipolar Profile Diagnostic Questionnaire, currently being validated.

With the intensification of the aging society, the incidence of various neurodegenerative diseases is on the rise. The hippocampus is susceptible to age-related neuronal decline and is the earliest and crucial region affected in the transition from healthy aging to neurodegenerative diseases. Before the diagnosis of neurodegenerative diseases, there is already a decline in brain energy metabolism, with the disruption of energy metabolism serving as the primary mechanism leading to neuronal damage. This triggers complex signaling mechanisms both inside and outside the brain during the aging process. Glucose serves as the primary energy source for brain tissues, and a decrease in glucose metabolism is an early indicator of age-related functional changes in the brain. Therefore, understanding the pathophysiological basis of glucose metabolism in the aging hippocampus, as well as the underlying mechanisms, is crucial in comprehending cognitive aging. Such understanding is integral for early intervention and the mitigation of memory and learning impairments caused by energy metabolism. In this review, we have delved into the characteristics of energy metabolism, focusing specifically on glucose metabolism, as well as exploring the molecular foundations and associated mechanisms present within hippocampal neuronal cells under both normal and aging conditions. Notably, our investigation has highlighted the vital roles played by ALG5 and STT3A, key molecules involved in N-glycosylation, in influencing GLUT expression and the rate of membrane transport, regulating glucose metabolism, and thereby influencing cellular glucose uptake. The exploration of this study direction holds considerable promise for future endeavors.

The interthalamic adhesion (IA), which may not be present in all humans, is a midline structure that connects the two thalami within the brain's third ventricle. A review of the known literature regarding the IA shows few histological studies and controversy regarding the organization of neurons within this region. This study conducted an anatomical investigation of the human IA in adult South African samples. Samples were obtained from 20 human adult embalmed cadavers: 11 from brains with a visible IA and 9 from brains without this feature. All the samples were harvested using sagittal sections of the area. Three additional samples were sectioned horizontally, yielding 33 tissue blocks. Before observation, these samples were appropriately processed for light microscopy and stained with haematoxylin and eosin, as well as cresyl violet. The results showed that no specific structural arrangements of the neurons were identifiable. The appearance appeared random, except for a distinguishable range in the frequency and dispersion of specific cells upon basic observation. Microglia were the most abundant cell type, and blood vessels were also observed. This study reports a novel inspection of the general histology of the thalamus, specifically of the IA and the periventricular (PVR) region, in midsagittal sections and three horizontal sections. This study confirmed the presence of pyramidal neurons within the IA, forming a bridge between the PVR region of the thalami, thus providing evidence to suggest that the IA could serve as a potential bridge for neural connections crossing over the brain's midline.