Search Results (3,408)

Curcumin is among the most well-studied natural substances, known for its biological actions within the central nervous system, its antioxidant and anti-inflammatory properties, and human health benefits. However, challenges persist in effectively utilising curcumin, addressing its metabolism and passage through the blood–brain barrier (BBB) in therapies targeting cerebrovascular diseases. Current challenges in curcumin’s applications revolve around its effects within neoplastic tissues alongside the development of intelligent formulations to enhance its bioavailability. Formulations have been discovered including curcumin’s complexes with brain-derived phospholipids and proteins, or its liposomal encapsulation. These novel strategies aim to improve curcumin’s bioavailability and stability, and its capability to cross the BBB, thereby potentially enhancing its efficacy in treating cerebrovascular diseases. In summary, this review provides a comprehensive overview of molecular pathways involved in interactions of curcumin and its metabolites, and brain vascular homeostasis. This review explores cellular and molecular current aspects, of curcumin-based effects with an emphasis on curcumin’s metabolism and its impact on pathological conditions, such as neurodegenerative diseases, schizophrenia, and cerebral angiopathy. It also highlights the limitations posed by curcumin’s poor bioavailability and discusses ongoing efforts to surpass these impediments to harness the full therapeutic potential of curcumin in neurological disorders. Full article

Background/Objectives: Cerebral palsy (CP) is a motor disorder resulting from brain damage that is common in childhood. Iron is vital for the body’s basic functions. Iron metabolism disorders and inflammation contribute to the neurological complications seen in CP. The purpose of this research was to ascertain the association and correlation between markers of inflammation and iron metabolism in children with CP. Methods: A total of 181 children diagnosed with CP and 111 typically developing children were retrospectively included in the study. Demographic data, blood parameters, C-reactive protein, iron, total iron binding capacity, and inflammation markers were evaluated. Results: C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR) and systemic immuno-inflammatory index (SII) levels of CP children were found to be statistically significantly higher than those of control group children (p < 0.05). Iron (Fe) and ferritin levels were lower in the CP group, while total iron binding capacity (TIBC) was higher. Spearman correlation analysis showed significant correlations between iron, ferritin and TIBC and SII. Conclusions: Iron deficiency and chronic inflammation are associated with the pathophysiology of CP in patients with CP, and therefore it is important to monitor markers of iron metabolism and inflammation in these patients. Full article

Premature deliveries and preterm newborns are of a special significance to obstetricians. Despite great improvement in neonatal intensive care in the last two decades, prematurity is still the leading cause of neonatal mortality and morbidity. Complications associated with premature deliveries are malpresentation, prolapse of the umbilical cord, entrapment of some parts of the fetal body, as well as severe bruising or bone fractures. The injuries may also include soft tissue damage, neurological injury, or intracranial hemorrhage. Small body weight as well as the unaccomplished development of fetal vital systems make preterm newborns vulnerable to delivery trauma. The main goal of a cesarean section in extremely preterm deliveries is to reduce the number of these complications. On the other hand, premature deliveries are associated with an undeveloped lower uterine segment and other difficulties encountered during the operation, which make the procedure more complicated and difficult to perform. Therefore, the preterm delivery or delivery of a fetus with growth retardation is of great concern. In our review, we investigated previous publications regarding en caul deliveries, mostly cesarean sections. We concentrated on the neonatal outcomes and tried to establish the optimal mode and time for a premature delivery. Full article

Background/Objectives: The Internet of Things (IoT) technology connects objects to the internet, and its applications are increasingly used in healthcare to improve the quality of care. However, the use of IoT for the nutritional management of patients with chronic neurological cognitive impairment is still in development. This scoping review aims to describe the integration of IoT and its applications to support monitoring, interventions, and nutritional education for patients with chronic neurological cognitive impairment. Methods: A scoping review was conducted using the Cochrane, PubMed/Medline, CINAHL, Embase, Scopus, and Web of Science databases following the Arksey and O’Malley framework. Results: Of the 1424 records identified, 10 were included in the review. Most of the articles were peer-reviewed proceedings from technology conferences or publications in scientific and technology journals. IoT-based innovations in nutritional management were discussed in methodological articles, case studies, or project descriptions. Innovations were identified across three key areas: monitoring, intervention, and education. Conclusions: IoT technology offers promising innovations for the nutritional management of patients with chronic neurological cognitive impairment. However, IoT capabilities in this field are still in the early stages of development and are not yet highly specific. Full article

Neurological disorders (NDs), such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and schizophrenia, represent a complex and multifaceted health challenge that affects millions of people around the world. Growing evidence suggests that disrupted neuronal calcium signalling contributes to the pathophysiology of NDs. Additionally, calcium functions as a ubiquitous second messenger involved in diverse cellular processes, from synaptic activity to intercellular communication, making it a potential therapeutic target. Recently, the development of the miniature fluorescence microscope (miniscope) enabled simultaneous recording of the spatiotemporal calcium activity from large neuronal ensembles in unrestrained animals, providing a novel method for studying NDs. In this review, we discuss the abnormalities observed in calcium signalling and its potential as a therapeutic target for NDs. Additionally, we highlight recent studies that utilise miniscope technology to investigate the alterations in calcium dynamics associated with NDs. Full article

Mutations in the GBA1 gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), are associated with Gaucher disease and increased risk of Parkinson’s disease. This study describes the discovery and characterization of novel allosteric pharmacological chaperones for GCase through an innovative computational approach combined with experimental validation. Utilizing virtual screening and structure-activity relationship optimization, researchers identified several compounds that significantly enhance GCase activity and stability across various cellular models, including patient-derived fibroblasts and neuronal cells harboring GBA1 mutations. Among these, compound 3 emerged as a lead candidate, demonstrating the ability to enhance GCase protein levels and enzymatic activity while effectively reducing the accumulation of toxic substrates in neuronal models. Importantly, pharmacokinetic studies revealed that compound 3 has favorable brain penetration, indicating its potential as a disease-modifying therapy for GBA1-related disorders affecting the central nervous system. This research not only offers a framework for developing allosteric GCase modulators but also unveils promising new therapeutic strategies for managing Gaucher disease and Parkinson’s disease. The ability of compound 3 to cross the blood-brain barrier emphasizes its potential significance in addressing neurological symptoms associated with these conditions. Full article

Background/Objectives: Military aviators can be exposed to extreme physiological stressors, including decompression stress, G-forces, as well as intermittent hypoxia and/or hyperoxia, which may contribute to neurobiological dysfunction/damage. This study aimed to investigate the levels of neurological biomarkers in military aviators to assess the potential risk of long-term brain injury and neurodegeneration. Methods: This cross-sectional study involved 48 Canadian Armed Forces (CAF) aviators and 48 non-aviator CAF controls. Plasma samples were analyzed for biomarkers of glial activation (GFAP), axonal damage (NF-L, pNF-H), oxidative stress (PRDX-6), and neurodegeneration (T-tau), along with S100b, NSE, and UCHL-1. The biomarker concentrations were quantified using multiplexed immunoassays. Results: The aviators exhibited significantly elevated levels of GFAP, NF-L, PRDX-6, and T-tau compared to the CAF controls (p < 0.001), indicating increased glial activation, axonal injury, and oxidative stress. Trends toward higher levels of S100b, NSE, and UCHL-1 were observed but were not statistically significant. The elevated biomarker levels suggest cumulative brain damage, raising concerns about potential long-term neurological impairments. Conclusions: Military aviators are at increased risk for neurobiological injury, including glial and axonal damage, oxidative stress, and early neurodegeneration. These findings emphasize the importance of proactive monitoring and further research to understand the long-term impacts of high-altitude flight on brain health and to develop strategies for mitigating cognitive decline and neurodegenerative risks in this population. Full article

Background: Radix Paeoniae Rubra (RPR), an edible and medicinal Traditional Chinese Medicine (TCM), is extensively employed in therapeutic interventions of cardiovascular and cerebrovascular diseases. However, the curative effect of RPR on ischemic stroke remains ambiguous. This work integrated network pharmacology, molecular docking, and experimental validation to explore the mechanisms of RPR in treating ischemic stroke. Methods: In this study, we preliminarily elucidated the therapeutic effect and mechanism of RPR on ischemic stroke through network pharmacology, molecular docking analysis, and experimental verification. Results: The results indicated that RPR improved the neurological deficit scores, decreased the size of infarcts, and reduced brain edema symptoms in the tMCAO mice model. Furthermore, through network pharmacology and molecular docking, four core targets (MAPK3, TNF-α, MAPK14, and JNK) closely related to RPR’s treatment of ischemic stroke were identified, exhibiting strong affinity with two key active components of RPR: albiflorin (AF) and β-sitosterol (BSS). The Western blot showed the potential mechanism of RPR treatment for ischemic stroke by regulating the MAPK signaling pathway. Moreover, RPR and its main active ingredients exhibited a significant inhibitory effect on platelets. Conclusion: In conclusion, this study revealed that RPR alleviates ischemic injury by activating the MAPK signaling pathway, and its protective effect may partly stem from inhibiting platelet activation. This work may provide a scientific basis for the development and utilization of RPR as a natural edible material to prevent ischemic stroke and anti-platelet therapy. Full article

The gut–brain axis plays an integral role in maintaining overall health, with growing evidence suggesting its impact on the development of various neuropsychiatric disorders, including depression. This review explores the complex relationship between gut microbiota and glutamate (Glu) regulation, highlighting its effect on brain health, particularly in the context of depression following certain neurological insults. We discuss how microbial populations can either facilitate or limit Glu uptake, influencing its bioavailability and predisposing to neuroinflammation and neurotoxicity. Additionally, we examine the role of gut metabolites and their influence on the blood–brain barrier and neurotransmitter systems involved in mood regulation. The therapeutic potential of microbiome-targeted interventions, such as fecal microbiota transplantation, is also highlighted. While much research has explored the role of Glu in major depressive disorders and other neurological diseases, the contribution of gut microbiota in post-neurological depression remains underexplored. Future research should focus on explaining the mechanisms linking the gut microbiota to neuropsychiatric outcomes, particularly in conditions such as post-stroke depression, post-traumatic brain-injury depression, and epilepsy-associated depression. Systematic reviews and human clinical studies are needed to establish causal relationships and assess the efficacy of microbiome-targeted therapies in improving the neuropsychiatric sequalae after neurological insults. Full article

Aim: This article aims to explore the role of the human gut microbiota (GM) in the pathogenesis of neurological, psychiatric, and neurodevelopmental disorders, highlighting its influence on health and disease, and investigating potential therapeutic strategies targeting GM modulation. Materials and Methods: A comprehensive analysis of the gut microbiota’s composition and its interaction with the human body, particularly, its role in neurological and psychiatric conditions, is provided. The review discusses factors influencing GM composition, including birth mode, breastfeeding, diet, medications, and geography. Additionally, it examines the GM’s functions, such as nutrient absorption, immune regulation, and pathogen defense, alongside its interactions with the nervous system through the gut–brain axis, neurotransmitters, and short-chain fatty acids (SCFAs). Results: Alterations in the GM are linked to various disorders, including Parkinson’s disease, multiple sclerosis, depression, schizophrenia, ADHD, and autism. The GM influences cognitive functions, stress responses, and mood regulation. Antibiotic use disrupts GM diversity, increasing the risk of metabolic disorders, obesity, and allergic diseases. Emerging therapies such as probiotics, prebiotics, and microbiota transplantation show promise in modulating the GM and alleviating symptoms of neurological and psychiatric conditions. Conclusions. The modulation of the GM represents a promising approach for personalized treatment strategies. Further research is needed to better understand the underlying mechanisms and to develop targeted therapies aimed at restoring GM balance for improved clinical outcomes. Full article

Background: Monoclonal antibodies approved by the FDA, lecanemab, donanemab, and aducanumab, are failing to meet the expected efficacy to treat early Alzheimer’s disease, and aducanumab has been recalled. Methods: Recently, it was reported that the clinical trials of these antibodies may have violated patient’s rights and subjected them to high, likely lethal risk. The challenge with developing antibodies to treat neurological disorders is their poor blood–brain barrier (BBB) penetration if the antibody must enter the brain, resulting in almost negligible brain bioavailability, requiring high dosing that can be toxic. Results: The reported efficacy of these drugs should also be reviewed, considering the placebo effects, since all antibodies have shown severe side effects that are not prevented by the placebo responses. In this critical and urgent advice to the FDA, I am suggesting a guideline amendment to all clinical trials requiring proof of sufficient brain bioavailability at the site of action, where it is known. Conclusions: For antibodies to cross the blood–brain barrier, there are proven options such as conjugating with transferrin protein, making clinical trials in its absence more questionable. Full article

Neonatal intraventricular hemorrhage is a serious condition associated with significant acute and long-term morbidity and mortality. Neurosurgical intervention aims to relieve life-threatening raised intracranial pressure and prevent neurological deterioration. In recent years, advancements in disease understanding have paved the way for clinicians to re-evaluate conventional approaches in the management of affected patients. Examples include various neurosurgical techniques to actively reduce blood products with a view to avoid the consequences of complex hydrocephalus and intraparenchymal injury in the developing brain. In this entry paper, we aim to provide an overview of the current perspectives, pathophysiology and management strategies for this difficult condition. Full article

The objective of this study was to describe an outbreak of equine herpesvirus-1 myeloencephalopathy (EHM) in a population of aged equids. The outbreak was linked to the introduction of five healthy non-resident horses 15 days prior to the first case of acute recumbency. This fulminant EHM outbreak was predisposed by the grouping of the 33 unvaccinated animals in two large pens with shared water and feed troughs. Fourteen horses (42.4%) developed neurological deficits within the first week of the outbreak. Four additional equids developed fever and respiratory signs (EHV-1 infection), while fifteen horses remained healthy. EHM was supported by the detection of EHV-1 N₇₅₂ in blood (n = 11) and/or nasal secretions (9). Three out of four equids with EHV-1 infection and two out of fifteen healthy horses tested qPCR-positive for EHV-1. All animals were managed in the field. EHM and EHV-1 equids were treated with a combination of antiherpetic, anti-inflammatory, and antithrombotic drugs. Six out of fourteen EHM horses (42.9%) were euthanized because of recumbence and the inability to stand with assistance or vestibular signs. Anti-EHV-1 total IgG and IgG 4/7 levels in acute serum samples showed no significant difference amongst the three disease groups (p > 0.05); however, antibody levels rose significantly between acute and convalescent serum samples for EHM (p = 0.0001) and EHV-1 equids (p = 0.02). This outbreak highlights a very high EHM attack and fatality rate in a population of aged equids and rapid spread of EHV-1, as the population shared common pens and feeding practices. The outbreak also showed that EHM cases can be managed in the field when referral to a hospital is not an option. Full article

Central nervous system (CNS) infections caused by SARS-CoV-2 are uncommon. This case report describes the clinical progression of a 92-year-old female who developed a persistent neuroinfection associated with SARS-CoV-2. The patient initially presented with progressive fatigue, catarrhal symptoms, and a fever (38.6 °C). Initial laboratory findings revealed hypoxemia (O₂ saturation 79.8%), acidosis (pH 7.3), an elevated C-reactive protein (CRP) level of 14.8 mg/L, and a high D-dimer level (2.15 µg/mL). Nasopharyngeal (NP) antigen and RT-PCR tests confirmed SARS-CoV-2 infection, and an NP swab also detected penicillin- and ampicillin-resistant Staphylococcus aureus. She was admitted for conservative management, including oxygen supplementation, IV fluids, and prophylactic anticoagulation. Subsequently, she developed neurological symptoms—lethargy, discoordination, and impaired communication—without signs of meningism. Cerebrospinal fluid (CSF) analysis identified SARS-CoV-2 RNA (Ct = 29) on RT-PCR, while bacterial cultures remained negative. Treatment was intensified to include 10% mannitol, dexamethasone, and empiric ceftriaxone. Despite these interventions, the patient remained somnolent, with a Glasgow Coma Scale (GCS) score of 10. Upon discharge, her GCS had improved to 14; however, she continued to experience lethargy and cognitive issues, commonly described as “brain fog”. Inflammatory markers remained elevated (CRP 23 mg/L) and repeat RT-PCR of CSF confirmed a persistent SARS-CoV-2 presence (Ct = 31). This case underscores the potential for SARS-CoV-2 to cause prolonged CNS involvement, leading to persistent neurological impairment despite standard therapy. Further research is essential to clarify the pathophysiology of and determine optimal management for SARS-CoV-2 neuroinfections. Full article

Background: The term “fetal programming” refers to the effects of endogenous and exogenous corticosteroids, whether received from the mother or the fetus, on brain development and the hypothalamic–pituitary–adrenal axis reset. The authors of this narrative review examine the WHO’s guidelines for prenatal corticosteroids in pregnant women who are at high risk of premature delivery. These guidelines are regarded as the best available for preventing late-life problems resulting from preterm. Methods: In order to find full-text publications published in peer-reviewed journals between 1990 and 2023 that were written in English, the authors searched PubMed, Scopus, Cochrane Library, and Web of Science. Results: The authors highlight the possible adverse long-term effects of prenatal corticosteroid medication on human brain development and function. This pharmacological feature is therapeutically significant because there is less evidence in the scientific literature regarding the potential role that the timing, mode, and dosage of exogenous steroid treatment may have in neurological illnesses down the road. Conclusions: The authors expect that these studies will shed light on the relationship between specially designed prenatal corticosteroid therapy and the molecular mechanisms underlying the prenatal programming of neurodevelopment in childhood and adulthood. Full article