NeuroSci最新文献

(1) Background: Choroid plexus papillomas (CPPs) are rare brain tumors that tend to occur in very young children. Mechanisms of CPP development remain unelucidated. Separately, the process of angiogenesis has been implicated in other primary brain tumors. We hypothesize that angiogenesis is a hallmark of CPP biology. This study aims to identify and validate angiogenic factors in CPPs. (2) Methods: Cerebrospinal fluid (CSF) and CPP tumor samples are collected. A multiplex immunoassay panel is used to identify differentially expressed cytokines in the CSF samples. Concurrently, patient-derived primary cell cultures and their supernatants are derived from CPP samples. Targeted proteome blot arrays and human umbilical vein endothelial cell (HUVEC) angiogenesis assays are used for validation studies. (3) Results: CSF profiling showed higher expressions of VEGF-A, MCP-1, MMP-1, TNF-α, and CD40L in CPP patient samples versus non-tumor controls. Next, assessment via online protein-protein network platforms reports that these cytokines are associated with endothelial cell regulation. Using an angiogenesis-focused approach, CPP-derived cell lines and supernatants showed similarly higher expressions of VEGF, MCP-1, and MMP-1. Next, sprouting of nodes and tubule formation were observed in HUVEC angiogenesis assay cultures when conditioned CPP cell culture media was added. (4) Conclusions: This proof-of-concept study demonstrates potential to explore angiogenesis in CPP.

S100β is a significant signaling molecule and biomarker that is primarily expressed in the brain. At low physiological concentrations, S100β induces astrocyte maturation, microglial migration, and neural proliferation. However, high concentrations activate inflammatory and pro-apoptotic pathways. Due to this dual role, increased research is being invested into the role of S100β in neuronal homeostasis and inflammation. In fact, increased S100β expression is seen in many neuropathologies including Alzheimer's disease, Parkinson's disease, cerebral ischemia, and traumatic brain injury. High S100β is generally associated with worsened disease outcome. Here, we provide an overview of the structure and role of S100β in various pathways, particularly in the context of neurological disorders. Modulation of S100β levels also holds promise as a therapeutic strategy. Micro-RNAs (miRNA) post-transcriptionally regulate gene expression and provide a novel approach reduce excess S100β protein. However, much of this research is still in its infancy. We outline current studies identifying miRNA in human and animal models of various neurological disorders. S100β itself has several predicted miRNA interactions although most have not yet been directly validated. Together, we compile the literature identifying S100β and miRNAs to guide future research in this field. We also comment on the feasibility and future uses of miRNA for pharmaceutical regulation of S100β, particularly for neurological treatments.

Background: Neuropathic pain (NP), resulting from damage to the somatosensory nervous system, affects 7-10% of the global population and remains poorly managed despite available therapies. Smoking has been associated with increased pain severity and disease burden, yet its role in neuropathy/NP has not been systematically reviewed. This systematic review synthesizes the existing literature on smoking status and its relationship with neuropathy/NP incidence, prevalence, and severity. Methods: The review was conducted in accordance with PRISMA guidelines and included studies that assessed smoking consumption, dependency, quantity, and cessation in individuals with neuropathy/NP. Summary estimates were stratified by exposure type, and pooled odds ratios and relative risks were calculated. Results: Across 62 studies comprising cohort, case-control, and cross-sectional designs, smoking was consistently associated with greater NP prevalence and pain severity. Smoking dependency was linked to increased incidence, while cessation was associated with reduced risk of NP. Despite considerable heterogeneity and risk of bias, particularly from subjective exposure measurement and inconsistent classification, this relationship remained statistically significant. Conclusions: Findings support the role of smoking as a modifiable risk factor in various etiologies of neuropathy/NP. Cessation may represent a low-cost, low-risk, low-tech adjunctive therapy; however, further robust cessation interventional trials are needed, particularly for less common infectious causes of chronic NP such as leprosy.

Background: Traumatic brain injury (TBI) remains a significant contributor to global mortality and long-term neurological disability. Accurate prognostic biomarkers are crucial for enhancing prognostic accuracy and guiding personalized clinical management.

Objective: This review assesses the prognostic value of arterial spin labeling (ASL), a non-invasive MRI technique, in adult and pediatric TBI, with a focus on quantitative cerebral blood flow (CBF) and arterial transit time (ATT) measures. A comprehensive literature search was conducted across PubMed, Embase, Scopus, and IEEE databases, including observational studies and clinical trials that applied ASL techniques (pCASL, PASL, VSASL, multi-PLD) in TBI patients with functional or cognitive outcomes, with outcome assessments conducted at least 3 months post-injury.

Results: ASL-derived CBF and ATT parameters demonstrate potential as prognostic indicators across both acute and chronic stages of TBI. Hypoperfusion patterns correlate with worse neurocognitive outcomes, while region-specific perfusion alterations are associated with affective symptoms. Multi-delay and velocity-selective ASL sequences enhance diagnostic sensitivity in TBI with heterogeneous perfusion dynamics. Compared to conventional perfusion imaging, ASL provides absolute quantification without contrast agents, making it suitable for repeated monitoring in vulnerable populations. ASL emerges as a promising prognostic biomarker for clinical use in TBI.

Conclusion: Integrating ASL into multiparametric models may improve risk stratification and guide individualized therapeutic strategies.

Introduction: Despite clinical evidence for efficacy, there has been minimal uptake of transcranial direct current stimulation (tDCS) for musculoskeletal conditions. Thus, our objective was to explore the perceptions and experiences of people living with lower-limb musculoskeletal injury as well as healthy physically active populations and relate this to the usage of tDCS and key aspects of tDCS design that would improve the capacity for implementation.

Methods: We conducted a qualitative descriptive study of 16 participants (44% women) using semi-structured focus groups to identify the descriptions and experiences of people living with lower-limb musculoskeletal injury and healthy physically active populations. A thematic template was used to create a coding structure. Codes were then grouped, and key themes were derived from the data.

Results: Four primary themes were identified from focus groups. These were (i) the impact of musculoskeletal injuries on health and quality of life, (ii) performance and injury recovery as facilitators to using tDCS, (iii) barriers and facilitators to tCDS application and (iv) design and aesthetic factors for a tDCS device.

Discussion: Our qualitative descriptive study identified four themes relevant to the successful implementation of tDCS into rehabilitative and performance practice. To increase the likelihood of successful tDCS implementation, these barriers should be addressed and facilitators promoted. This should include innovative approaches to device application and structure that allow for a stylish, user-friendly design.

Optimal sensorimotor control depends on response timing. With age, it is broadly assumed that reaction time (RT) increases as cognitive function declines. However, it is not clear if the literature supports this assumption. The purpose of this work was to review the association between cognition and upper extremity RT in older adults. We conducted a search using Scopus database with four inclusion criteria: (1) healthy, community-dwelling adults over 60 years old, (2) upper extremity movement, (3) cognitive assessment, and (4) RT measure. Twenty-five of the 1608 articles screened met the inclusion criteria. Only nine studies directly or indirectly assessed the association between cognition and RT. Our interpretation of the literature was further limited by inconsistency in test selection and measurement interdependence that could be addressed by future studies. We present a conceptual framework to guide research assessing the influence of cognition on sensorimotor control with age.

(1) Background: Evidence from non-human animal and spaceflight analog studies have suggested that traveling to outer space could have a significant impact on the structural properties of the hippocampus, a brain region within the medial temporal lobe that is critical for learning and memory. Here, we tested this hypothesis in a group of astronauts who participated in a six-month mission in the International Space Station (ISS). (2) Methods: We collected magnetic resonance imaging (MRI) scans from a sample of 17 (9 males, 8 females) astronauts before and after the ISS mission, and calculated percent gray matter volume changes in the whole hippocampus and its (anterior, body, and posterior) subregions in both hemispheres. (3) Following the six-month mission in the ISS, we found a significantly decreased volume in the whole left hippocampus; in addition, when looking at subregions separately, we detected a significantly decreased volume in the anterior subregion of the left hippocampus and the body subregion of the right hippocampus. We also found a significantly decreased volume in the whole right hippocampus of male astronauts as compared to female astronauts. (4) Conclusions: This study, providing the very first evidence of hippocampal volumetric changes in astronauts following a six-month mission to the ISS, could have significant implications for cognitive performance during future long-duration spaceflights.

Amyotrophic lateral sclerosis (ALS) remains a progressive neurodegenerative disease, lacking effective causal therapies. The Wobbler mouse model harboring a spontaneous autosomal recessive mutation in the vacuolar protein sorting associated protein (Vps54), has emerged as a valuable model for investigating ALS pathophysiology and potential treatments. This model exhibits cellular and phenotypic parallels to human ALS, including protein aggregation, microglia and astrocyte activation, as well as characteristic disease progression at distinct stages. Exploring the underlying pathomechanisms and identifying therapeutic targets requires a comprehensive analysis of gene and protein expression. In this study, we examined the expression of three well-established housekeeping genes and proteins-calnexin, ß-actin, and ßIII-tubulin-in the cervical spinal cord of the Wobbler model. These candidates were selected based on their demonstrated stability across various systems like animal models or cell culture. Calnexin, an integral protein of the endoplasmic reticulum, ß-actin, a structural component of the cytoskeleton, and ß-tubulin III, a component of microtubules, were quantitatively assessed using quantitative reverse transcription-polymerase chain reaction (RT-PCR) for gene expression and Western blotting for protein expression. Our results revealed no significant differences in the expression of CANX, ACTB, and TUBB3 between spinal cords of wild-type and Wobbler mice at the symptomatic stage (p40) at both the gene and protein levels. These findings suggest that the pathophysiological alterations induced by the Wobbler mutation do not significantly affect the expression of these crucial housekeeping genes and proteins at p40. Overall, this study provides a basis for further investigations using the Wobbler mouse model, while highlighting the potential use of calnexin, ß-actin, and ßIII-tubulin as reliable reference genes and proteins in future research to aid in the discovery for effective therapeutic interventions.

Human memory is inherently susceptible to errors, including the formation of false memories-instances where individuals mistakenly recall information they were never exposed to. While prior research has largely focused on neural activity associated with false memory, the structural brain correlates of this phenomenon remain relatively unexplored. This study bridges that gap by investigating gray matter structure as it relates to individual differences in false memory performance. Using publicly available magnetic resonance imaging datasets, we analyzed cortical thickness (CT) in neural regions implicated in memory processes. To assess false memory, we applied signal detection theory, which provides a robust framework for differentiating between true and false memory. Our findings reveal that increased CT in the parietal lobe and middle occipital gyrus correlates with greater susceptibility to false memories, highlighting its role in integrating and manipulating memory information. Conversely, CT in the middle frontal gyrus and occipital pole was associated with enhanced accuracy in memory recall, emphasizing its importance in perceptual processing and encoding true memories. These results provide novel insights into the structural basis of memory errors and offer a foundation for future investigations into the neural underpinnings of memory reliability.

Pulsed radiofrequency (PRF) current applied to peripheral nerves is a modality used in interventional pain medicine, but its underlying mechanisms remain unclear. This study aimed to investigate whether ex vivo exposure of human monocytic THP-1 cells to PRF current or to heat induces β-endorphin production.

Methods: THP-1 cells were exposed to PRF current for 15 min or incubated at elevated temperatures (42 °C to 50 °C) for 3 or 15 min. Flow cytometry was used to assess cell viability, and β-endorphin concentrations in culture supernatants were quantified by ELISA. In a separate experiment, cells were stimulated with lipopolysaccharide (LPS) to compare its effects on β-endorphin release.

Results: A 3 min exposure to temperatures ≥ 46 °C reduced THP-1 cell viability, whereas a 15 min exposure to PRF current or to heat at 42 °C did not impair viability. Both PRF current and mild heat significantly enhanced β-endorphin release. β-Endorphin levels in the supernatant of LPS-stimulated cells were comparable to those of cells exposed to PRF current.

Conclusions: Ex vivo application of PRF current or mild heat enhanced β-endorphin production from THP-1 cells without significant cytotoxicity. These preliminary findings warrant further investigation using primary human monocytes and in vivo models to assess therapeutic potential.