Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted t...Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.展开更多
Neurodevelopmental and neurodegenerative illnesses constitute a global health issue and a foremost economic burden since they are a large cause of incapacity and death worldwide.Altogether,the burden of neurological d...Neurodevelopmental and neurodegenerative illnesses constitute a global health issue and a foremost economic burden since they are a large cause of incapacity and death worldwide.Altogether,the burden of neurological disorders has increased considerably over the past 30 years because of population aging.Overall,neurological diseases significantly impair cognitive and motor functions and their incidence will increase as societies age and the world's population continues to grow.Autism spectrum disorder,motor neuron disease,encephalopathy,epilepsy,stroke,ataxia,Alzheimer's disease,amyotrophic lateral sclerosis,Huntington's disease,and Parkinson's disease represent a non-exhaustive list of neurological illnesses.These affections are due to perturbations in cellular homeostasis leading to the progressive injury and death of neurons in the nervous system.Among the common features of neurological handicaps,we find protein aggregation,oxidative stress,neuroinflammation,and mitochondrial impairment in the target tissues,e.g.,the brain,cerebellum,and spinal cord.The high energy requirements of neurons and their inability to produce sufficient adenosine triphosphate by glycolysis,are responsible for their dependence on functional mitochondria for their integrity.Reactive oxygen species,produced along with the respiration process within mitochondria,can lead to oxidative stress,which compromises neuronal survival.Besides having an essential role in energy production and oxidative stress,mitochondria are indispensable for an array of cellular processes,such as amino acid metabolism,iron-sulfur cluster biosynthesis,calcium homeostasis,intrinsic programmed cell death(apoptosis),and intraorganellar signaling.Despite the progress made in the last decades in the understanding of a growing number of genetic and molecular causes of central nervous diseases,therapies that are effective to diminish or halt neuronal dysfunction/death are rare.Given the genetic complexity responsible for neurological disorders,the development of neuroprotective strategies seeking to preserve mitochondrial homeostasis is a realistic challenge to lastingly diminish the harmful evolution of these pathologies and so to recover quality of life.A promising candidate is the neuroglobin,a globin superfamily member of 151 amino acids,which is found at high levels in the brain,the eye,and the cerebellum.The protein,which localizes to mitochondria,is involved in electron transfer,oxygen storage and defence against oxidative stress;hence,possessing neuroprotective properties.This review surveys up-to-date knowledge and emphasizes on existing investigations regarding neuroglobin physiological functions,which remain since its discovery in 2000 under intense debate and the possibility of using neuroglobin either by gene therapy or its direct delivery into the brain to treat neurological disorders.展开更多
With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely o...With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely obesity and neurodegeneration.展开更多
BACKGROUND Stress hyperglycemia(SH)is a common phenomenon that is present in about 50%of patients with acute ischemic stroke(AIS).It is thought to be a main risk factor for poor functional outcome among patients with ...BACKGROUND Stress hyperglycemia(SH)is a common phenomenon that is present in about 50%of patients with acute ischemic stroke(AIS).It is thought to be a main risk factor for poor functional outcome among patients with AIS undergoing intravenous thrombolysis(IVT).AIM To investigate the predictive value of glycemic indicators for early neurological outcomes(ENOs)in patients with AIS treated with IVT.METHODS We retrospectively reviewed a prospectively collected database of patients with AIS who underwent IVT at the Department of Neurology,Second Affiliated Hospital of Xuzhou Medical University,between January 2017 and June 2022.ENO included early neurological improvement(ENI)and early neurological deterioration(END),defined as a decrease or increase in the National Institutes of Health Stroke Scale(NIHSS)score between baseline and 24 hours after IVT.We analyzed the associations between glycemic indicators[including admission hyperglycemia(AH),fasting blood glucose(FBG),and SH ratio(SHR)]and ENO in all patients and in subgroups stratified by diabetes mellitus(DM).RESULTS A total of 819 patients with AIS treated with IVT were included.Among these,AH was observed in 329 patients(40.2%).Compared with patients without AH,those with AH were more likely to have a higher prevalence of DM(P<0.001)and hypertension(P=0.031)and presented with higher admission NIHSS scores(P<0.001).During the first 24 hours after IVT,END occurred in 208 patients(25.4%)and ENI occurred in 156 patients(19.0%).Multivariate mixed logistic regression analyses indicated that END was independently associated with AH[odds ratio(OR):1.744,95%confidence interval(CI):1.236-2.463;P=0.002].Subjects were classified into four groups representing quartiles.Compared with Q1,patients in the higher quartiles of SHR(Q2:OR:2.306,95%CI:1.342-3.960;P=0.002)(Q3:OR:2.284,95%CI:1.346-3.876;P=0.002)(Q4:OR:3.486,95%CI:2.088-5.820;P=0.001)and FBG(Q3:OR:1.746,95%CI:1.045-2.917;P=0.033)(Q4:OR:2.436,95%CI:1.476-4.022;P=0.001)had a significantly higher risk of END in the overall population.However,none of the glycemic indicators were found to be associated with ENI in patients with or without DM.CONCLUSION Our study demonstrated that glycemic indicators in patients with stroke treated with IVT were associated with the presence of END rather than ENI during the first 24 hours after admission.展开更多
Alcohol use disorder(AUD)is a medical condition that impairs a person's ability to stop or manage their drinking in the face of negative social,occupational,or health consequences.AUD is defined by the National In...Alcohol use disorder(AUD)is a medical condition that impairs a person's ability to stop or manage their drinking in the face of negative social,occupational,or health consequences.AUD is defined by the National Institute on Alcohol Abuse and Alcoholism as a"severe problem".The central nervous system is the primary target of alcohol's adverse effects.It is crucial to identify various neurological disorders associated with AUD,including alcohol withdrawal syndrome,Wernicke-Korsakoff syndrome,Marchiafava-Bignami disease,dementia,and neuropathy.To gain a better understanding of the neurological environment of alcoholism and to shed light on the role of various neurotransmitters in the phenomenon of alcoholism.A comprehensive search of online databases,including PubMed,EMBASE,Web of Science,and Google Scholar,was conducted to identify relevant articles.Several neurotransmitters(dopamine,gammaaminobutyric acid,serotonin,and glutamate)have been linked to alcoholism due to a brain imbalance.Alcoholism appears to be a complex genetic disorder,with variations in many genes influencing risk.Some of these genes have been identified,including two alcohol metabolism genes,alcohol dehydrogenase 1B gene and aldehyde dehydrogenase 2 gene,which have the most potent known effects on the risk of alcoholism.Neuronal degeneration and demyelination in people with AUD may be caused by neuronal damage,nutrient deficiencies,and blood brain barrier dysfunction;however,the underlying mechanism is unknown.This review will provide a detailed overview of the neurobiology of alcohol addiction,followed by recent studies published in the genetics of alcohol addiction,molecular mechanism and detailed information on the various acute and chronic neurological manifestations of alcoholism for the Future research.展开更多
Ferroptosis is a form of cell death elicited by an imbalance in intracellular iron concentrations,leading to enhanced lipid peroxidation.In neurological disorders,both oxidative stress and mitochondrial damage can con...Ferroptosis is a form of cell death elicited by an imbalance in intracellular iron concentrations,leading to enhanced lipid peroxidation.In neurological disorders,both oxidative stress and mitochondrial damage can contribute to ferroptosis,resulting in nerve cell dysfunction and death.The ubiquitin-proteasome system(UPS)refers to a cellular pathway in which specific proteins are tagged with ubiquitin for recognition and degradation by the proteasome.In neuro-logical conditions,the UPS plays a significant role in regu-lating ferroptosis.In this review,we outline how the UPS regulates iron metabolism,ferroptosis,and their interplay in neurological diseases.In addition,we discuss the future application of small-molecule inhibitors and identify poten-tial drug targets.Further investigation into the mechanisms of UPS-mediated ferroptosis will provide novel insights and strategies for therapeutic interventions and clinical applica-tions in neurological diseases.展开更多
The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central n...The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central nervous system, with sensory stimulation and excitation conduction functions. Astrocytes and microglia belong to the glial cell family, which is the main source of cytokines and represents the main defense system of the central nervous system. Nerve cells undergo neurotransmission or gliotransmission, which regulates neuronal activity via the ion channels, receptors, or transporters expressed on nerve cell membranes. Ion channels, composed of large transmembrane proteins, play crucial roles in maintaining nerve cell homeostasis. These channels are also important for control of the membrane potential and in the secretion of neurotransmitters. A variety of cellular functions and life activities, including functional regulation of the central nervous system, the generation and conduction of nerve excitation, the occurrence of receptor potential, heart pulsation, smooth muscle peristalsis, skeletal muscle contraction, and hormone secretion, are closely related to ion channels associated with passive transmembrane transport. Two types of ion channels in the central nervous system, potassium channels and calcium channels, are closely related to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and epilepsy. Accordingly, various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders. In this review, we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease, Alzheimer's disease, depression, epilepsy, autism, and rare disorders. We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders. We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions. Although a few novel ion-channelspecific modulators have been discovered, meaningful therapies have largely not yet been realized. The lack of target-specific drugs, their requirement to cross the blood–brain barrier, and their exact underlying mechanisms all need further attention. This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.展开更多
Recent advances in research on extracellular vesicles have significantly enhanced their potential as therapeutic agents for neurological diseases.Owing to their therapeutic properties and ability to cross the blood–b...Recent advances in research on extracellular vesicles have significantly enhanced their potential as therapeutic agents for neurological diseases.Owing to their therapeutic properties and ability to cross the blood–brain barrier,extracellular vesicles are recognized as promising drug delivery vehicles for various neurological conditions,including ischemic stroke,traumatic brain injury,neurodegenerative diseases,glioma,and psychosis.However,the clinical application of natural extracellular vesicles is hindered by their limited targeting ability and short clearance from the body.To address these limitations,multiple engineering strategies have been developed to enhance the targeting capabilities of extracellular vesicles,thereby enabling the delivery of therapeutic contents to specific tissues or cells.Therefore,this review aims to highlight the latest advancements in natural and targeting-engineered extracellular vesicles,exploring their applications in treating traumatic brain injury,ischemic stroke,Parkinson's disease,Alzheimer's disease,amyotrophic lateral sclerosis,glioma,and psychosis.Additionally,we summarized recent clinical trials involving extracellular vesicles and discussed the challenges and future prospects of using targeting-engineered extracellular vesicles for drug delivery in treating neurological diseases.This review offers new insights for developing highly targeted therapies in this field.展开更多
BACKGROUND Functional neurological disorder(FND)in children is a complex and multifaceted condition characterized by neurological symptoms that cannot be explained by organic pathology.Despite its prevalence,FND in pe...BACKGROUND Functional neurological disorder(FND)in children is a complex and multifaceted condition characterized by neurological symptoms that cannot be explained by organic pathology.Despite its prevalence,FND in pediatric populations remains under-researched,with challenges in diagnosis and management AIM To synthesize the current literature on FND in children,focusing on clinical presentation,diagnostic approaches,treatment strategies,and outcomes.METHODS A comprehensive literature search was conducted across multiple databases,including PubMed,Scopus,and Web of Science,for articles published up to August 2024.Studies were included if they addressed FND in pediatric populations,specifically focusing on review articles,research articles,systematic reviews,meta-analyses,case reports,guidelines,expert opinions,and editorials.Data extraction and quality assessment were performed according to PRISMA guidelines.A total of 308 articles were included in the final analysis.RESULTS The analysis included 189 review articles,57 research articles,3 systematic reviews and meta-analyses,5 case reports,2 guidelines,5 expert opinions,and 2 editorials.Key findings revealed a broad spectrum of symptoms,including motor and sensory disturbances and psychological factors contributing to the onset and persistence of FND.Diagnostic challenges were frequently highlighted,emphasizing the need for interdisciplinary approaches.Treatment strategies varied,with cognitive-behavioral therapy(CBT)and multidisciplinary care emerging as the most effective approaches.The outcomes varied,with early intervention being critical for a better prognosis.CONCLUSION Early diagnosis and multidisciplinary care,including CBT,are critical for improving outcomes in pediatric FND.Standardized diagnostic criteria and treatment protocols are needed to enhance clinical management.展开更多
Retraction Note to:Neurosci.Bull.(2019)35:461-470 https://doi.org/10.1007/s12264-018-00333-w The Editor-in-Chief has retracted this article.After publication,concerns were raised regarding image similarities across pu...Retraction Note to:Neurosci.Bull.(2019)35:461-470 https://doi.org/10.1007/s12264-018-00333-w The Editor-in-Chief has retracted this article.After publication,concerns were raised regarding image similarities across publications from unrelated authors.Specifically.展开更多
BACKGROUND Pancreas transplantation(PT)has emerged as a critical therapeutic intervention for patients with type 1 diabetes mellitus(T1DM).This procedure restores neuroendocrine communication,which is essential for op...BACKGROUND Pancreas transplantation(PT)has emerged as a critical therapeutic intervention for patients with type 1 diabetes mellitus(T1DM).This procedure restores neuroendocrine communication,which is essential for optimal pancreatic function and insulin regulation.The recovery process involves multiple phases,including neural regeneration,revascularization,and the re-establishment of synaptic connections,all of which contribute to the restoration of both endocrine and neurological functions.AIM To systematically examine the mechanisms underlying neurological recovery following PT,to explore the role of endocrine factors in restoring neurofunctional integrity,and to evaluate the impact of immunosuppressive therapy on nerve regeneration and its clinical outcomes.METHODS A comprehensive literature search was conducted across international databases such as PubMed,Web of Science,and Cochrane Library to identify studies addressing PT,neurological recovery,and endocrine regulation.Inclusion criteria encompassed randomized controlled trials,cohort studies,and systematic reviews.The review focused on the neurogenic mechanisms activated post-transplantation,the effect of glycemic control on nerve repair,and the implications of immunosuppressive drugs on the process of neurological recovery.RESULTS A total of 211 articles were initially identified through the literature search across international databases such as PubMed,Web of Science,and Cochrane Library.Following a detailed evaluation and the application of inclusion and exclusion criteria,56 articles were further reviewed,and 8 were selected for the final analysis.Additionally,a comprehensive patent search yielded 168 patents,out of which 6 were selected for further examination.These sources,including both journal literature and patents,offer significant insights into the mechanisms of neurological recovery and endocrine function following PT,with an emphasis on nerve regeneration,glycemic control,and the impact of immunosuppressive therapy.CONCLUSION PT represents a promising intervention for restoring both endocrine and neurological functions in patients with T1DM.Glycemic control,neural regeneration,and the restoration of neuroendocrine signaling are key components of successful recovery.While the procedure yields substantial improvements in nerve function,challenges persist,particularly in patients with long-standing diabetes or severe neuropathy.The dual impact of immunosuppressive drugs on immune suppression and neurotoxicity necessitates careful management.Future research should focus on refining immunosuppressive protocols and exploring advanced therapeutic options,including stem cell-based interventions,to enhance neural regeneration and further improve clinical outcomes.展开更多
BACKGROUND Artificial intelligence(AI)has become significantly integrated into healthcare,particularly in the diag-nosing of neurological disorders.This advancement has enabled neurologists and physicians to diagnose ...BACKGROUND Artificial intelligence(AI)has become significantly integrated into healthcare,particularly in the diag-nosing of neurological disorders.This advancement has enabled neurologists and physicians to diagnose conditions more quickly and effectively,ultimately benefiting patients.AIM To explore the current status and key highlights of AI-related articles in diagnosing of neurological disorders.METHODS A systematic literature review was conducted in the Web of Science Core Collection database using the following strategy:TS=("Artificial Intelligence"OR"Computational Intelligence"OR"Machine Learning"OR"AI")AND TS=("Neurological disorders"OR"CNS disorder"AND"diagnosis").The search was limited to articles and reviews.Microsoft Excel 2019 and VOSviewer were utilized to identify major contributors,including authors,institutions,countries,and journals.Additionally,VOSviewer was employed to analyze and visualize current trends and hot topics through network visualization maps.RESULTS A total of 276 publications from 2000 to 2024 were retrieved.The United States,India,and China emerged as the top contributors in this field.Major institutions included Johns Hopkins University,King's College London,and Harvard Medical School.The most prolific author was U.Rajendra Acharya from the University of Southern Queensland(Australia).Among journals,IEEE Access,Scientific Reports,and Sensors were the most productive,while Frontiers in Neuroscience led in total citations.Central topics in AI-related articles on neurological disorders diagnosis included Alzheimer's disease,Parkinson's disease,dementia,epilepsy,autism,attention deficit hyperactivity disorder,and their intersections with deep learning and AI.CONCLUSION Research on AI's role in diagnosing neurological disorders is becoming widely recognized for its growing importance.AI shows promise in diagnosing various neurological disorders,yet requires further improvement and extensive future research.展开更多
Objective:To evaluate the predictive value of Modified Early Warning Score(MEWS)for neurological disease prognosis and identify prognostic factors.Methods:This retrospective study analyzed 768 neurological patients wi...Objective:To evaluate the predictive value of Modified Early Warning Score(MEWS)for neurological disease prognosis and identify prognostic factors.Methods:This retrospective study analyzed 768 neurological patients with MEWS≥4(June 2022–June 2024).Patients were stratified by outcomes(favorable/unfavorable).Multivariable logistic regression and ROC analysis were performed.Results:108 cases(13.1%)had unfavorable outcomes.Significant prognostic factors included:age,TBI history,onset-to-admission time,PT,MEWS score,and MEWS≥4 frequency(all P<0.05).MEWS showed AUC=0.749(sensitivity 62.0%,specificity 77.4%).Conclusion:MEWS demonstrates moderate predictive value(AUC=0.749)for neurological outcomes.Consciousness assessment limitations(56.5%impaired cases)may affect sensitivity.A specialized model incorporating pupillary reflexes and GCS is recommended for improved early warning.展开更多
BACKGROUND The neurological and psychiatric sequelae of coronavirus disease 2019(COVID-19)have been documented,yet further data are needed to thoroughly evaluate the impact of COVID-19 on brain health years after the ...BACKGROUND The neurological and psychiatric sequelae of coronavirus disease 2019(COVID-19)have been documented,yet further data are needed to thoroughly evaluate the impact of COVID-19 on brain health years after the infection.AIM To examine whether COVID-19 infection is associated with exacerbation,recurrence,or progression of pre-existing neurological or psychiatric disorders-a highrisk population that is underrepresented in COVID-19 outcome research in National Guard Health Affair patients in 4-years following a COVID-19 diagnosis.METHODS For this multicenter retrospective cohort study,we used data from the National Guard hospitals electronic health records network(BestCare)with over 10 million patients.Our cohort comprised patients who had a COVID-19 diagnosis;a matched control cohort included patient did not expose to COVID-19 in same period.Age and sex were matching factors.We estimated the incidence of 14 neurological and psychiatric outcomes in nearly 4 years after a confirmed diagnosis of COVID-19.Using a multiple logistic regression,we compared incidences with those in propensity score-matched cohorts of patients with no exposure to COVID-19.Ramadan M et al.Neurological and psychiatric risks post-COVID-19 RESULTS Our primary cohort comprised 4437 patients diagnosed with COVID-19,and our propensity-score 1:1 matched control cohort comprised 4437 individuals.Nearly two-third of the COVID-19 cohort(71%)were diagnosed in 2020,and 2021.The most prevalent diagnoses for both cohorts were epilepsy 30.68%,mood disorder 23.92%,and nerve plexus disorder 22.13%.Dementia was nearly 4 times higher among COVID-19 cohort(8.27%)compared to the control cohort(2.57%).Five neurological and psychiatric outcomes had odds ratios(OR)that were significantly higher than 1 for people who had COVID-19 compared to people who had never been infected.These outcomes were cognitive deficit OR=1.54,95%confidence interval(CI):1.23-1.91,P=0.0001;nerve plexus disorder OR=1.13,95%CI:1.01-1.25,P=0.02;substance use disorder OR=1.95,95%CI:1.12-3.38,P=0.01;mood disorder OR=1.16,95%CI:1.05-1.29,P=0.003;and anxiety disorder OR=1.39,95%CI:1.07-1.79,P=0.01.CONCLUSION The study highlights the persistent risk of neurological and psychiatric conditions in COVID-19 survivors up to four years post-infection.Although the incidence was lower than in previous large studies,long-term consequences remain significant,emphasizing the need for ongoing monitoring and support in mental health and neurological care.展开更多
γ neuromodulation has emerged as a promising strategy for addressing neurological and psychiatric disorders,particularly in regulating executive and cognitive functions.This review explores the latest neuromodulation...γ neuromodulation has emerged as a promising strategy for addressing neurological and psychiatric disorders,particularly in regulating executive and cognitive functions.This review explores the latest neuromodulation techniques,focusing on the critical role of γ oscillations in various brain disorders.Direct γ neuromodulation induces γ -frequency oscillations to synchronize disrupted brain networks,while indirect methods influence γ oscillations by modulating cortical excitability.We investigate how monitoring dynamic features of γ oscillations allows for detailed evaluations of neuromodulation effectiveness.By targeting γ oscillatory patterns and restoring healthy cross-frequency coupling,interventions may alleviate cognitive and behavioral symptoms linked to disrupted communication.This review examines clinical applications of γ neuromodulations,including enhancing cognitive function through 40 Hz multisensory stimulation in Alzheimer’s disease,improving motor function in Parkinson’s disease,controlling seizures in epilepsy,and modulating emotional dysfunctions in depression.Additionally,these neuromodulation strategies aim to regulate excitatory-inhibitory imbalances and restore γ synchrony across neurological and psychiatric disorders.The review highlights the potential of γ oscillations as biomarkers to boost restorative results in clinical applications of neuromodulation.Future studies might focus on integrating multimodal personalized protocols,artificial intelligence(AI)driven frameworks for neural decoding,and global multicenter collaborations to standardize and scale precision treatments across diverse disorders.展开更多
BACKGROUND Acute cerebral infarction(ACI),a leading cause of death and disability,causes brain ischemia due to vessel blockage.Current time-limited interventions,such as clot removal,often fail to restore full functio...BACKGROUND Acute cerebral infarction(ACI),a leading cause of death and disability,causes brain ischemia due to vessel blockage.Current time-limited interventions,such as clot removal,often fail to restore full function.Neurorestoration is vital,but complicated.Vascular endothelial growth factor(VEGF)and basic fibroblast growth factor(bFGF)promote angiogenesis and neuroprotection.Stem cell therapy has potential to promote neurorestoration.Specifically,neural stem cells(NSC)reconstruct neural tissue,while mesenchymal stem cells(MSCs)provide support and secrete beneficial factors.Combining NSCs and MSCs in stem cell therapy may synergistically enhance ACI recovery,potentially via the regulation of VEGF and bFGF.However,the mechanisms underlying this combined approach remain unclear.AIM To investigate the therapeutic effect of combined NSC and MSC transplantation on neurological recovery and bFGF/VEGF expression in ACI patients.METHODS This study enrolled 156 patients with ACI treated from June 2022 to June 2023.Patients were randomly assigned to two groups:The control group(n=78)received conventional drug therapy,while the observation group(n=78)received conventional therapy and combined NSC and MSC transplantation.The following outcomes were compared between groups:National Institutes of Health Stroke Scale(NIHSS)score,Barthel index,cerebral perfusion and diffusion on magnetic resonance imaging,serum bFGF and VEGF levels,clinical efficacy,and adverse events.RESULTS Serum VEGF and bFGF levels negatively correlated with NIHSS scores in patients with ACI(r=-0.388,r=-0.239;P<0.05).The observation group(NSC and MSC)showed a significantly higher clinical efficacy of treatment than the controls(85.9%vs 69.2%;P<0.05).Both groups showed improved cerebral perfusion,increased Barthel index,and decreased NIHSS scores post-treatment(P<0.05),with significantly greater improvements in the observation group.Serum VEGF and bFGF levels increased significantly in both groups(P<0.05),but were higher in the observation group.Adverse events in the observation group(transient fever:4 cases;agitation:1 case;headache:2 cases)were mild and resolved with symptomatic treatment.Six-month follow-up revealed no abnormalities in magnetic resonance imaging,electrocardiogram,or blood tests.CONCLUSION NSC-MSC combination therapy enhances neurological function and cerebral perfusion in patients with ACI by upregulating VEGF and bFGF expression,demonstrating favorable clinical efficacy and safety.展开更多
BACKGROUND:Iron metabolism dyshomeostasis is associated with ferroptosis and ischemiareperfusion injury.We aim to investigate post-cardiac arrest changes in plasma iron metabolism-related parameters and their prognost...BACKGROUND:Iron metabolism dyshomeostasis is associated with ferroptosis and ischemiareperfusion injury.We aim to investigate post-cardiac arrest changes in plasma iron metabolism-related parameters and their prognostic value for 28-day neurological outcomes.METHODS:In this prospective observational cohort study,plasma iron metabolism-related parameters(iron,ferritin,hepcidin,soluble transferrin receptor[sTfR],total iron binding capacity[TIBC],and transferrin saturation),interleukin-6,and neuron-specific enolase(NSE)were assessed in 120 patients after restoration of spontaneous circulation(ROSC)on days 1 and 3 of intensive care unit(ICU)admission and in 40 healthy controls.The primary outcome was poor 28-day neurological prognosis.RESULTS:Compared to controls,post-ROSC patients exhibited significant plasma iron metabolism disturbances,including decreased iron,TIBC,transferrin saturation,with elevated hepcidin,ferritin,sTfR,interleukin-6,and NSE on day 1 after ICU admission(P<0.05 for all).On day 28 post-ROSC,patients with poor neurological outcomes(71/120)presented more pronounced alterations than those with good neurological outcomes.Binary logistic analysis revealed that a plasma iron concentration≤11.2μmol/L(odds ratio[OR]0.607,95% confidence interval[CI]0.455-0.808)and an NSE concentration≥20.5 ng/mL(OR 1.020,95%CI 1.005-1.035)on day 1 of ICU admission were associated with 28-day poor neurological outcomes.The plasma iron-NSE combination showed better predictive performance(area under the curve=0.935,sensitivity 89.8%,specificity 84.5%).CONCLUSION:Early post-ROSC plasma iron metabolism disturbances combined with NSE elevation were associated with the 28-day neurological prognosis,suggesting the therapeutic potential of targeting the iron metabolism pathway.展开更多
Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein functio...Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein function or structure,understanding their genetic basis is crucial for accurate diagnosis and targeted therapies.To investigate the underlying pathogenesis of these conditions,researchers often use non-mammalian model organisms,such as Drosophila(fruit flies),which is valued for their genetic manipulability,cost-efficiency,and preservation of genes and biological functions across evolutionary time.Genetic tools available in Drosophila,including CRISPR-Cas9,offer a means to manipulate gene expression,allowing for a deep exploration of the genetic underpinnings of rare neurological diseases.Drosophila boasts a versatile genetic toolkit,rapid generation turnover,and ease of large-scale experimentation,making it an invaluable resource for identifying potential drug candidates.Researchers can expose flies carrying disease-associated mutations to various compounds,rapidly pinpointing promising therapeutic agents for further investigation in mammalian models and,ultimately,clinical trials.In this comprehensive review,we explore rare neurological diseases where fly research has significantly contributed to our understanding of their genetic basis,pathophysiology,and potential therapeutic implications.We discuss rare diseases associated with both neuron-expressed and glial-expressed genes.Specific cases include mutations in CDK19 resulting in epilepsy and developmental delay,mutations in TIAM1 leading to a neurodevelopmental disorder with seizures and language delay,and mutations in IRF2BPL causing seizures,a neurodevelopmental disorder with regression,loss of speech,and abnormal movements.And we explore mutations in EMC1 related to cerebellar atrophy,visual impairment,psychomotor retardation,and gain-of-function mutations in ACOX1 causing Mitchell syndrome.Loss-of-function mutations in ACOX1 result in ACOX1 deficiency,characterized by very-long-chain fatty acid accumulation and glial degeneration.Notably,this review highlights how modeling these diseases in Drosophila has provided valuable insights into their pathophysiology,offering a platform for the rapid identification of potential therapeutic interventions.Rare neurological diseases involve a wide range of expression systems,and sometimes common phenotypes can be found among different genes that cause abnormalities in neurons or glia.Furthermore,mutations within the same gene may result in varying functional outcomes,such as complete loss of function,partial loss of function,or gain-of-function mutations.The phenotypes observed in patients can differ significantly,underscoring the complexity of these conditions.In conclusion,Drosophila represents an indispensable and cost-effective tool for investigating rare neurological diseases.By facilitating the modeling of these conditions,Drosophila contributes to a deeper understanding of their genetic basis,pathophysiology,and potential therapies.This approach accelerates the discovery of promising drug candidates,ultimately benefiting patients affected by these complex and understudied diseases.展开更多
Objective:To analyze the clinical application and effects of the body restraint reduction program for severe neurological patients.Methods:A total of 206 patients admitted to the neurology department of the hospital f...Objective:To analyze the clinical application and effects of the body restraint reduction program for severe neurological patients.Methods:A total of 206 patients admitted to the neurology department of the hospital from January 2022 to May 2025 were selected as the research subjects.Among them,102 patients from January 2022 to May 2025 were assigned to the observation group,and 104 patients during the same period served as the control group.In practice,the control group received conventional body restraint,while the observation group adopted the reduction program.The incidence of unplanned extubation and restraint-related complications were compared between the two groups.Results:The body restraint rate and complication rate in the observation group were significantly lower(P<0.05).After nurse training,their knowledge mastery and operational ability were significantly higher than before training(P<0.01).Conclusion:The body restraint reduction program for severe neurological patients can effectively reduce the restraint rate and complication incidence,while helping improve nurses’restraint management capabilities,serving as an effective means to enhance overall nursing quality.展开更多
Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic ...Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic brain injury remains poorly understood.In this study,we established rat models of moderate traumatic brain injury using Feeney's weight-dropping method and treated them using rTMS.To help determine the mechanism of action,we measured levels of seve ral impo rtant brain activity-related proteins and their mRNA.On the injured side of the brain,we found that rTMS increased the protein levels and mRNA expression of brain-derived neurotrophic factor,tropomyosin receptor kinase B,N-methyl-D-aspartic acid receptor 1,and phosphorylated cAMP response element binding protein,which are closely associated with the occurrence of long-term potentiation.rTMS also partially reve rsed the loss of synaptophysin after injury and promoted the remodeling of synaptic ultrastructure.These findings suggest that upregulation of synaptic plasticity-related protein expression is the mechanism through which rTMS promotes neurological function recovery after moderate traumatic brain injury.展开更多
基金supported by the National Natural Science Foundation of China,Nos.32271389,31900987(both to PY)the Natural Science Foundation of Jiangsu Province,No.BK20230608(to JJ)。
文摘Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.
基金supported by AFM-Telethon grants N°21704 and 23264,Universite Paris Cite(Paris)the National Institute of Health and Medical Research(INSERM)+3 种基金the National Center for Scientific Research(CNRS)the French Association Connaître les Syndromes Cerebelleux(CSC)(to MCD)GV/2021/188 granted from Conselleria of Innovation,Universities,28 Science and Society digital of the Community of Valencia(Spain)(to ITC)Subprograma Atraccion de Talento-Contratos Postdoctorales de la Universitat de Valencia(to IMY).
文摘Neurodevelopmental and neurodegenerative illnesses constitute a global health issue and a foremost economic burden since they are a large cause of incapacity and death worldwide.Altogether,the burden of neurological disorders has increased considerably over the past 30 years because of population aging.Overall,neurological diseases significantly impair cognitive and motor functions and their incidence will increase as societies age and the world's population continues to grow.Autism spectrum disorder,motor neuron disease,encephalopathy,epilepsy,stroke,ataxia,Alzheimer's disease,amyotrophic lateral sclerosis,Huntington's disease,and Parkinson's disease represent a non-exhaustive list of neurological illnesses.These affections are due to perturbations in cellular homeostasis leading to the progressive injury and death of neurons in the nervous system.Among the common features of neurological handicaps,we find protein aggregation,oxidative stress,neuroinflammation,and mitochondrial impairment in the target tissues,e.g.,the brain,cerebellum,and spinal cord.The high energy requirements of neurons and their inability to produce sufficient adenosine triphosphate by glycolysis,are responsible for their dependence on functional mitochondria for their integrity.Reactive oxygen species,produced along with the respiration process within mitochondria,can lead to oxidative stress,which compromises neuronal survival.Besides having an essential role in energy production and oxidative stress,mitochondria are indispensable for an array of cellular processes,such as amino acid metabolism,iron-sulfur cluster biosynthesis,calcium homeostasis,intrinsic programmed cell death(apoptosis),and intraorganellar signaling.Despite the progress made in the last decades in the understanding of a growing number of genetic and molecular causes of central nervous diseases,therapies that are effective to diminish or halt neuronal dysfunction/death are rare.Given the genetic complexity responsible for neurological disorders,the development of neuroprotective strategies seeking to preserve mitochondrial homeostasis is a realistic challenge to lastingly diminish the harmful evolution of these pathologies and so to recover quality of life.A promising candidate is the neuroglobin,a globin superfamily member of 151 amino acids,which is found at high levels in the brain,the eye,and the cerebellum.The protein,which localizes to mitochondria,is involved in electron transfer,oxygen storage and defence against oxidative stress;hence,possessing neuroprotective properties.This review surveys up-to-date knowledge and emphasizes on existing investigations regarding neuroglobin physiological functions,which remain since its discovery in 2000 under intense debate and the possibility of using neuroglobin either by gene therapy or its direct delivery into the brain to treat neurological disorders.
文摘With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely obesity and neurodegeneration.
基金Supported by the Foundation of Jiangsu Provincial Commission of Health and Family Planning,No.QNRC2016353the Commission of Health and Family Planning Xuzhou,No.KC22206.
文摘BACKGROUND Stress hyperglycemia(SH)is a common phenomenon that is present in about 50%of patients with acute ischemic stroke(AIS).It is thought to be a main risk factor for poor functional outcome among patients with AIS undergoing intravenous thrombolysis(IVT).AIM To investigate the predictive value of glycemic indicators for early neurological outcomes(ENOs)in patients with AIS treated with IVT.METHODS We retrospectively reviewed a prospectively collected database of patients with AIS who underwent IVT at the Department of Neurology,Second Affiliated Hospital of Xuzhou Medical University,between January 2017 and June 2022.ENO included early neurological improvement(ENI)and early neurological deterioration(END),defined as a decrease or increase in the National Institutes of Health Stroke Scale(NIHSS)score between baseline and 24 hours after IVT.We analyzed the associations between glycemic indicators[including admission hyperglycemia(AH),fasting blood glucose(FBG),and SH ratio(SHR)]and ENO in all patients and in subgroups stratified by diabetes mellitus(DM).RESULTS A total of 819 patients with AIS treated with IVT were included.Among these,AH was observed in 329 patients(40.2%).Compared with patients without AH,those with AH were more likely to have a higher prevalence of DM(P<0.001)and hypertension(P=0.031)and presented with higher admission NIHSS scores(P<0.001).During the first 24 hours after IVT,END occurred in 208 patients(25.4%)and ENI occurred in 156 patients(19.0%).Multivariate mixed logistic regression analyses indicated that END was independently associated with AH[odds ratio(OR):1.744,95%confidence interval(CI):1.236-2.463;P=0.002].Subjects were classified into four groups representing quartiles.Compared with Q1,patients in the higher quartiles of SHR(Q2:OR:2.306,95%CI:1.342-3.960;P=0.002)(Q3:OR:2.284,95%CI:1.346-3.876;P=0.002)(Q4:OR:3.486,95%CI:2.088-5.820;P=0.001)and FBG(Q3:OR:1.746,95%CI:1.045-2.917;P=0.033)(Q4:OR:2.436,95%CI:1.476-4.022;P=0.001)had a significantly higher risk of END in the overall population.However,none of the glycemic indicators were found to be associated with ENI in patients with or without DM.CONCLUSION Our study demonstrated that glycemic indicators in patients with stroke treated with IVT were associated with the presence of END rather than ENI during the first 24 hours after admission.
文摘Alcohol use disorder(AUD)is a medical condition that impairs a person's ability to stop or manage their drinking in the face of negative social,occupational,or health consequences.AUD is defined by the National Institute on Alcohol Abuse and Alcoholism as a"severe problem".The central nervous system is the primary target of alcohol's adverse effects.It is crucial to identify various neurological disorders associated with AUD,including alcohol withdrawal syndrome,Wernicke-Korsakoff syndrome,Marchiafava-Bignami disease,dementia,and neuropathy.To gain a better understanding of the neurological environment of alcoholism and to shed light on the role of various neurotransmitters in the phenomenon of alcoholism.A comprehensive search of online databases,including PubMed,EMBASE,Web of Science,and Google Scholar,was conducted to identify relevant articles.Several neurotransmitters(dopamine,gammaaminobutyric acid,serotonin,and glutamate)have been linked to alcoholism due to a brain imbalance.Alcoholism appears to be a complex genetic disorder,with variations in many genes influencing risk.Some of these genes have been identified,including two alcohol metabolism genes,alcohol dehydrogenase 1B gene and aldehyde dehydrogenase 2 gene,which have the most potent known effects on the risk of alcoholism.Neuronal degeneration and demyelination in people with AUD may be caused by neuronal damage,nutrient deficiencies,and blood brain barrier dysfunction;however,the underlying mechanism is unknown.This review will provide a detailed overview of the neurobiology of alcohol addiction,followed by recent studies published in the genetics of alcohol addiction,molecular mechanism and detailed information on the various acute and chronic neurological manifestations of alcoholism for the Future research.
基金supported by the 2024 Talent Project of Shandong First Medical University(045RC200008)the Taishan Scholars Program(tsqn202211225).
文摘Ferroptosis is a form of cell death elicited by an imbalance in intracellular iron concentrations,leading to enhanced lipid peroxidation.In neurological disorders,both oxidative stress and mitochondrial damage can contribute to ferroptosis,resulting in nerve cell dysfunction and death.The ubiquitin-proteasome system(UPS)refers to a cellular pathway in which specific proteins are tagged with ubiquitin for recognition and degradation by the proteasome.In neuro-logical conditions,the UPS plays a significant role in regu-lating ferroptosis.In this review,we outline how the UPS regulates iron metabolism,ferroptosis,and their interplay in neurological diseases.In addition,we discuss the future application of small-molecule inhibitors and identify poten-tial drug targets.Further investigation into the mechanisms of UPS-mediated ferroptosis will provide novel insights and strategies for therapeutic interventions and clinical applica-tions in neurological diseases.
基金supported by the National Natural Science Foundation of China,Nos.81901098(to TC),82201668(to HL)Fujian Provincial Health Technology Project,No.2021QNA072(to HL)。
文摘The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central nervous system, with sensory stimulation and excitation conduction functions. Astrocytes and microglia belong to the glial cell family, which is the main source of cytokines and represents the main defense system of the central nervous system. Nerve cells undergo neurotransmission or gliotransmission, which regulates neuronal activity via the ion channels, receptors, or transporters expressed on nerve cell membranes. Ion channels, composed of large transmembrane proteins, play crucial roles in maintaining nerve cell homeostasis. These channels are also important for control of the membrane potential and in the secretion of neurotransmitters. A variety of cellular functions and life activities, including functional regulation of the central nervous system, the generation and conduction of nerve excitation, the occurrence of receptor potential, heart pulsation, smooth muscle peristalsis, skeletal muscle contraction, and hormone secretion, are closely related to ion channels associated with passive transmembrane transport. Two types of ion channels in the central nervous system, potassium channels and calcium channels, are closely related to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and epilepsy. Accordingly, various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders. In this review, we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease, Alzheimer's disease, depression, epilepsy, autism, and rare disorders. We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders. We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions. Although a few novel ion-channelspecific modulators have been discovered, meaningful therapies have largely not yet been realized. The lack of target-specific drugs, their requirement to cross the blood–brain barrier, and their exact underlying mechanisms all need further attention. This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.
基金supported by the National Natural Science Foundation of China,Nos.82171363,82371381(to PL),82171458(to XJ)Key Research and Development Project of Shaa nxi Province,Nos.2024SF-YBXM-404(to KY)。
文摘Recent advances in research on extracellular vesicles have significantly enhanced their potential as therapeutic agents for neurological diseases.Owing to their therapeutic properties and ability to cross the blood–brain barrier,extracellular vesicles are recognized as promising drug delivery vehicles for various neurological conditions,including ischemic stroke,traumatic brain injury,neurodegenerative diseases,glioma,and psychosis.However,the clinical application of natural extracellular vesicles is hindered by their limited targeting ability and short clearance from the body.To address these limitations,multiple engineering strategies have been developed to enhance the targeting capabilities of extracellular vesicles,thereby enabling the delivery of therapeutic contents to specific tissues or cells.Therefore,this review aims to highlight the latest advancements in natural and targeting-engineered extracellular vesicles,exploring their applications in treating traumatic brain injury,ischemic stroke,Parkinson's disease,Alzheimer's disease,amyotrophic lateral sclerosis,glioma,and psychosis.Additionally,we summarized recent clinical trials involving extracellular vesicles and discussed the challenges and future prospects of using targeting-engineered extracellular vesicles for drug delivery in treating neurological diseases.This review offers new insights for developing highly targeted therapies in this field.
文摘BACKGROUND Functional neurological disorder(FND)in children is a complex and multifaceted condition characterized by neurological symptoms that cannot be explained by organic pathology.Despite its prevalence,FND in pediatric populations remains under-researched,with challenges in diagnosis and management AIM To synthesize the current literature on FND in children,focusing on clinical presentation,diagnostic approaches,treatment strategies,and outcomes.METHODS A comprehensive literature search was conducted across multiple databases,including PubMed,Scopus,and Web of Science,for articles published up to August 2024.Studies were included if they addressed FND in pediatric populations,specifically focusing on review articles,research articles,systematic reviews,meta-analyses,case reports,guidelines,expert opinions,and editorials.Data extraction and quality assessment were performed according to PRISMA guidelines.A total of 308 articles were included in the final analysis.RESULTS The analysis included 189 review articles,57 research articles,3 systematic reviews and meta-analyses,5 case reports,2 guidelines,5 expert opinions,and 2 editorials.Key findings revealed a broad spectrum of symptoms,including motor and sensory disturbances and psychological factors contributing to the onset and persistence of FND.Diagnostic challenges were frequently highlighted,emphasizing the need for interdisciplinary approaches.Treatment strategies varied,with cognitive-behavioral therapy(CBT)and multidisciplinary care emerging as the most effective approaches.The outcomes varied,with early intervention being critical for a better prognosis.CONCLUSION Early diagnosis and multidisciplinary care,including CBT,are critical for improving outcomes in pediatric FND.Standardized diagnostic criteria and treatment protocols are needed to enhance clinical management.
文摘Retraction Note to:Neurosci.Bull.(2019)35:461-470 https://doi.org/10.1007/s12264-018-00333-w The Editor-in-Chief has retracted this article.After publication,concerns were raised regarding image similarities across publications from unrelated authors.Specifically.
基金Supported by National Natural Science Foundation of China,No.82305376The Project of Supporting Young Scientific and Technological Talents in Jiangsu Province in 2024,No.JSTJ-2024-380.
文摘BACKGROUND Pancreas transplantation(PT)has emerged as a critical therapeutic intervention for patients with type 1 diabetes mellitus(T1DM).This procedure restores neuroendocrine communication,which is essential for optimal pancreatic function and insulin regulation.The recovery process involves multiple phases,including neural regeneration,revascularization,and the re-establishment of synaptic connections,all of which contribute to the restoration of both endocrine and neurological functions.AIM To systematically examine the mechanisms underlying neurological recovery following PT,to explore the role of endocrine factors in restoring neurofunctional integrity,and to evaluate the impact of immunosuppressive therapy on nerve regeneration and its clinical outcomes.METHODS A comprehensive literature search was conducted across international databases such as PubMed,Web of Science,and Cochrane Library to identify studies addressing PT,neurological recovery,and endocrine regulation.Inclusion criteria encompassed randomized controlled trials,cohort studies,and systematic reviews.The review focused on the neurogenic mechanisms activated post-transplantation,the effect of glycemic control on nerve repair,and the implications of immunosuppressive drugs on the process of neurological recovery.RESULTS A total of 211 articles were initially identified through the literature search across international databases such as PubMed,Web of Science,and Cochrane Library.Following a detailed evaluation and the application of inclusion and exclusion criteria,56 articles were further reviewed,and 8 were selected for the final analysis.Additionally,a comprehensive patent search yielded 168 patents,out of which 6 were selected for further examination.These sources,including both journal literature and patents,offer significant insights into the mechanisms of neurological recovery and endocrine function following PT,with an emphasis on nerve regeneration,glycemic control,and the impact of immunosuppressive therapy.CONCLUSION PT represents a promising intervention for restoring both endocrine and neurological functions in patients with T1DM.Glycemic control,neural regeneration,and the restoration of neuroendocrine signaling are key components of successful recovery.While the procedure yields substantial improvements in nerve function,challenges persist,particularly in patients with long-standing diabetes or severe neuropathy.The dual impact of immunosuppressive drugs on immune suppression and neurotoxicity necessitates careful management.Future research should focus on refining immunosuppressive protocols and exploring advanced therapeutic options,including stem cell-based interventions,to enhance neural regeneration and further improve clinical outcomes.
文摘BACKGROUND Artificial intelligence(AI)has become significantly integrated into healthcare,particularly in the diag-nosing of neurological disorders.This advancement has enabled neurologists and physicians to diagnose conditions more quickly and effectively,ultimately benefiting patients.AIM To explore the current status and key highlights of AI-related articles in diagnosing of neurological disorders.METHODS A systematic literature review was conducted in the Web of Science Core Collection database using the following strategy:TS=("Artificial Intelligence"OR"Computational Intelligence"OR"Machine Learning"OR"AI")AND TS=("Neurological disorders"OR"CNS disorder"AND"diagnosis").The search was limited to articles and reviews.Microsoft Excel 2019 and VOSviewer were utilized to identify major contributors,including authors,institutions,countries,and journals.Additionally,VOSviewer was employed to analyze and visualize current trends and hot topics through network visualization maps.RESULTS A total of 276 publications from 2000 to 2024 were retrieved.The United States,India,and China emerged as the top contributors in this field.Major institutions included Johns Hopkins University,King's College London,and Harvard Medical School.The most prolific author was U.Rajendra Acharya from the University of Southern Queensland(Australia).Among journals,IEEE Access,Scientific Reports,and Sensors were the most productive,while Frontiers in Neuroscience led in total citations.Central topics in AI-related articles on neurological disorders diagnosis included Alzheimer's disease,Parkinson's disease,dementia,epilepsy,autism,attention deficit hyperactivity disorder,and their intersections with deep learning and AI.CONCLUSION Research on AI's role in diagnosing neurological disorders is becoming widely recognized for its growing importance.AI shows promise in diagnosing various neurological disorders,yet requires further improvement and extensive future research.
基金Research on the Measurement of Pulmonary Compliance and Its Guided Therapeutic Efficacy Analysis in Patients with ARDS Secondary to Severe Multiple Injuries(Project No.:XSD2023002)。
文摘Objective:To evaluate the predictive value of Modified Early Warning Score(MEWS)for neurological disease prognosis and identify prognostic factors.Methods:This retrospective study analyzed 768 neurological patients with MEWS≥4(June 2022–June 2024).Patients were stratified by outcomes(favorable/unfavorable).Multivariable logistic regression and ROC analysis were performed.Results:108 cases(13.1%)had unfavorable outcomes.Significant prognostic factors included:age,TBI history,onset-to-admission time,PT,MEWS score,and MEWS≥4 frequency(all P<0.05).MEWS showed AUC=0.749(sensitivity 62.0%,specificity 77.4%).Conclusion:MEWS demonstrates moderate predictive value(AUC=0.749)for neurological outcomes.Consciousness assessment limitations(56.5%impaired cases)may affect sensitivity.A specialized model incorporating pupillary reflexes and GCS is recommended for improved early warning.
文摘BACKGROUND The neurological and psychiatric sequelae of coronavirus disease 2019(COVID-19)have been documented,yet further data are needed to thoroughly evaluate the impact of COVID-19 on brain health years after the infection.AIM To examine whether COVID-19 infection is associated with exacerbation,recurrence,or progression of pre-existing neurological or psychiatric disorders-a highrisk population that is underrepresented in COVID-19 outcome research in National Guard Health Affair patients in 4-years following a COVID-19 diagnosis.METHODS For this multicenter retrospective cohort study,we used data from the National Guard hospitals electronic health records network(BestCare)with over 10 million patients.Our cohort comprised patients who had a COVID-19 diagnosis;a matched control cohort included patient did not expose to COVID-19 in same period.Age and sex were matching factors.We estimated the incidence of 14 neurological and psychiatric outcomes in nearly 4 years after a confirmed diagnosis of COVID-19.Using a multiple logistic regression,we compared incidences with those in propensity score-matched cohorts of patients with no exposure to COVID-19.Ramadan M et al.Neurological and psychiatric risks post-COVID-19 RESULTS Our primary cohort comprised 4437 patients diagnosed with COVID-19,and our propensity-score 1:1 matched control cohort comprised 4437 individuals.Nearly two-third of the COVID-19 cohort(71%)were diagnosed in 2020,and 2021.The most prevalent diagnoses for both cohorts were epilepsy 30.68%,mood disorder 23.92%,and nerve plexus disorder 22.13%.Dementia was nearly 4 times higher among COVID-19 cohort(8.27%)compared to the control cohort(2.57%).Five neurological and psychiatric outcomes had odds ratios(OR)that were significantly higher than 1 for people who had COVID-19 compared to people who had never been infected.These outcomes were cognitive deficit OR=1.54,95%confidence interval(CI):1.23-1.91,P=0.0001;nerve plexus disorder OR=1.13,95%CI:1.01-1.25,P=0.02;substance use disorder OR=1.95,95%CI:1.12-3.38,P=0.01;mood disorder OR=1.16,95%CI:1.05-1.29,P=0.003;and anxiety disorder OR=1.39,95%CI:1.07-1.79,P=0.01.CONCLUSION The study highlights the persistent risk of neurological and psychiatric conditions in COVID-19 survivors up to four years post-infection.Although the incidence was lower than in previous large studies,long-term consequences remain significant,emphasizing the need for ongoing monitoring and support in mental health and neurological care.
基金supported by the National Natural Science Foundation of China(82401829)the Leading Innovative and Entrepreneur Team Introduction Program of Zhejiang(2023R01002).
文摘γ neuromodulation has emerged as a promising strategy for addressing neurological and psychiatric disorders,particularly in regulating executive and cognitive functions.This review explores the latest neuromodulation techniques,focusing on the critical role of γ oscillations in various brain disorders.Direct γ neuromodulation induces γ -frequency oscillations to synchronize disrupted brain networks,while indirect methods influence γ oscillations by modulating cortical excitability.We investigate how monitoring dynamic features of γ oscillations allows for detailed evaluations of neuromodulation effectiveness.By targeting γ oscillatory patterns and restoring healthy cross-frequency coupling,interventions may alleviate cognitive and behavioral symptoms linked to disrupted communication.This review examines clinical applications of γ neuromodulations,including enhancing cognitive function through 40 Hz multisensory stimulation in Alzheimer’s disease,improving motor function in Parkinson’s disease,controlling seizures in epilepsy,and modulating emotional dysfunctions in depression.Additionally,these neuromodulation strategies aim to regulate excitatory-inhibitory imbalances and restore γ synchrony across neurological and psychiatric disorders.The review highlights the potential of γ oscillations as biomarkers to boost restorative results in clinical applications of neuromodulation.Future studies might focus on integrating multimodal personalized protocols,artificial intelligence(AI)driven frameworks for neural decoding,and global multicenter collaborations to standardize and scale precision treatments across diverse disorders.
文摘BACKGROUND Acute cerebral infarction(ACI),a leading cause of death and disability,causes brain ischemia due to vessel blockage.Current time-limited interventions,such as clot removal,often fail to restore full function.Neurorestoration is vital,but complicated.Vascular endothelial growth factor(VEGF)and basic fibroblast growth factor(bFGF)promote angiogenesis and neuroprotection.Stem cell therapy has potential to promote neurorestoration.Specifically,neural stem cells(NSC)reconstruct neural tissue,while mesenchymal stem cells(MSCs)provide support and secrete beneficial factors.Combining NSCs and MSCs in stem cell therapy may synergistically enhance ACI recovery,potentially via the regulation of VEGF and bFGF.However,the mechanisms underlying this combined approach remain unclear.AIM To investigate the therapeutic effect of combined NSC and MSC transplantation on neurological recovery and bFGF/VEGF expression in ACI patients.METHODS This study enrolled 156 patients with ACI treated from June 2022 to June 2023.Patients were randomly assigned to two groups:The control group(n=78)received conventional drug therapy,while the observation group(n=78)received conventional therapy and combined NSC and MSC transplantation.The following outcomes were compared between groups:National Institutes of Health Stroke Scale(NIHSS)score,Barthel index,cerebral perfusion and diffusion on magnetic resonance imaging,serum bFGF and VEGF levels,clinical efficacy,and adverse events.RESULTS Serum VEGF and bFGF levels negatively correlated with NIHSS scores in patients with ACI(r=-0.388,r=-0.239;P<0.05).The observation group(NSC and MSC)showed a significantly higher clinical efficacy of treatment than the controls(85.9%vs 69.2%;P<0.05).Both groups showed improved cerebral perfusion,increased Barthel index,and decreased NIHSS scores post-treatment(P<0.05),with significantly greater improvements in the observation group.Serum VEGF and bFGF levels increased significantly in both groups(P<0.05),but were higher in the observation group.Adverse events in the observation group(transient fever:4 cases;agitation:1 case;headache:2 cases)were mild and resolved with symptomatic treatment.Six-month follow-up revealed no abnormalities in magnetic resonance imaging,electrocardiogram,or blood tests.CONCLUSION NSC-MSC combination therapy enhances neurological function and cerebral perfusion in patients with ACI by upregulating VEGF and bFGF expression,demonstrating favorable clinical efficacy and safety.
基金funded by the Shenzhen Key Medical Discipline Construction Fund(SZXK046)the Shenzhen Science and Technology Program(JCYJ20230807112007014).
文摘BACKGROUND:Iron metabolism dyshomeostasis is associated with ferroptosis and ischemiareperfusion injury.We aim to investigate post-cardiac arrest changes in plasma iron metabolism-related parameters and their prognostic value for 28-day neurological outcomes.METHODS:In this prospective observational cohort study,plasma iron metabolism-related parameters(iron,ferritin,hepcidin,soluble transferrin receptor[sTfR],total iron binding capacity[TIBC],and transferrin saturation),interleukin-6,and neuron-specific enolase(NSE)were assessed in 120 patients after restoration of spontaneous circulation(ROSC)on days 1 and 3 of intensive care unit(ICU)admission and in 40 healthy controls.The primary outcome was poor 28-day neurological prognosis.RESULTS:Compared to controls,post-ROSC patients exhibited significant plasma iron metabolism disturbances,including decreased iron,TIBC,transferrin saturation,with elevated hepcidin,ferritin,sTfR,interleukin-6,and NSE on day 1 after ICU admission(P<0.05 for all).On day 28 post-ROSC,patients with poor neurological outcomes(71/120)presented more pronounced alterations than those with good neurological outcomes.Binary logistic analysis revealed that a plasma iron concentration≤11.2μmol/L(odds ratio[OR]0.607,95% confidence interval[CI]0.455-0.808)and an NSE concentration≥20.5 ng/mL(OR 1.020,95%CI 1.005-1.035)on day 1 of ICU admission were associated with 28-day poor neurological outcomes.The plasma iron-NSE combination showed better predictive performance(area under the curve=0.935,sensitivity 89.8%,specificity 84.5%).CONCLUSION:Early post-ROSC plasma iron metabolism disturbances combined with NSE elevation were associated with the 28-day neurological prognosis,suggesting the therapeutic potential of targeting the iron metabolism pathway.
基金supported by Warren Alpert Foundation and Houston Methodist Academic Institute Laboratory Operating Fund(to HLC).
文摘Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein function or structure,understanding their genetic basis is crucial for accurate diagnosis and targeted therapies.To investigate the underlying pathogenesis of these conditions,researchers often use non-mammalian model organisms,such as Drosophila(fruit flies),which is valued for their genetic manipulability,cost-efficiency,and preservation of genes and biological functions across evolutionary time.Genetic tools available in Drosophila,including CRISPR-Cas9,offer a means to manipulate gene expression,allowing for a deep exploration of the genetic underpinnings of rare neurological diseases.Drosophila boasts a versatile genetic toolkit,rapid generation turnover,and ease of large-scale experimentation,making it an invaluable resource for identifying potential drug candidates.Researchers can expose flies carrying disease-associated mutations to various compounds,rapidly pinpointing promising therapeutic agents for further investigation in mammalian models and,ultimately,clinical trials.In this comprehensive review,we explore rare neurological diseases where fly research has significantly contributed to our understanding of their genetic basis,pathophysiology,and potential therapeutic implications.We discuss rare diseases associated with both neuron-expressed and glial-expressed genes.Specific cases include mutations in CDK19 resulting in epilepsy and developmental delay,mutations in TIAM1 leading to a neurodevelopmental disorder with seizures and language delay,and mutations in IRF2BPL causing seizures,a neurodevelopmental disorder with regression,loss of speech,and abnormal movements.And we explore mutations in EMC1 related to cerebellar atrophy,visual impairment,psychomotor retardation,and gain-of-function mutations in ACOX1 causing Mitchell syndrome.Loss-of-function mutations in ACOX1 result in ACOX1 deficiency,characterized by very-long-chain fatty acid accumulation and glial degeneration.Notably,this review highlights how modeling these diseases in Drosophila has provided valuable insights into their pathophysiology,offering a platform for the rapid identification of potential therapeutic interventions.Rare neurological diseases involve a wide range of expression systems,and sometimes common phenotypes can be found among different genes that cause abnormalities in neurons or glia.Furthermore,mutations within the same gene may result in varying functional outcomes,such as complete loss of function,partial loss of function,or gain-of-function mutations.The phenotypes observed in patients can differ significantly,underscoring the complexity of these conditions.In conclusion,Drosophila represents an indispensable and cost-effective tool for investigating rare neurological diseases.By facilitating the modeling of these conditions,Drosophila contributes to a deeper understanding of their genetic basis,pathophysiology,and potential therapies.This approach accelerates the discovery of promising drug candidates,ultimately benefiting patients affected by these complex and understudied diseases.
文摘Objective:To analyze the clinical application and effects of the body restraint reduction program for severe neurological patients.Methods:A total of 206 patients admitted to the neurology department of the hospital from January 2022 to May 2025 were selected as the research subjects.Among them,102 patients from January 2022 to May 2025 were assigned to the observation group,and 104 patients during the same period served as the control group.In practice,the control group received conventional body restraint,while the observation group adopted the reduction program.The incidence of unplanned extubation and restraint-related complications were compared between the two groups.Results:The body restraint rate and complication rate in the observation group were significantly lower(P<0.05).After nurse training,their knowledge mastery and operational ability were significantly higher than before training(P<0.01).Conclusion:The body restraint reduction program for severe neurological patients can effectively reduce the restraint rate and complication incidence,while helping improve nurses’restraint management capabilities,serving as an effective means to enhance overall nursing quality.
基金supported by the President Foundation of Nanfang Hospital,Southern Medical University,No.2016Z003(50107021)(to JZF).
文摘Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic brain injury remains poorly understood.In this study,we established rat models of moderate traumatic brain injury using Feeney's weight-dropping method and treated them using rTMS.To help determine the mechanism of action,we measured levels of seve ral impo rtant brain activity-related proteins and their mRNA.On the injured side of the brain,we found that rTMS increased the protein levels and mRNA expression of brain-derived neurotrophic factor,tropomyosin receptor kinase B,N-methyl-D-aspartic acid receptor 1,and phosphorylated cAMP response element binding protein,which are closely associated with the occurrence of long-term potentiation.rTMS also partially reve rsed the loss of synaptophysin after injury and promoted the remodeling of synaptic ultrastructure.These findings suggest that upregulation of synaptic plasticity-related protein expression is the mechanism through which rTMS promotes neurological function recovery after moderate traumatic brain injury.
