Serum glial fibrillary acidic protein (sGFAP) is increasingly studied as a biomarker of astroglial injury, but comparative data between ultra-sensitive analytical platforms are limited. This study evaluated the agreement between the newly developed VEUS technology and the established single-molecule array (SIMOA) method.
Methods
A single-centre retrospective analysis was conducted at the Department of Neurology, University Hospital Ostrava. Patients ≥18 years with relapsing-remitting multiple sclerosis, non-inflammatory neurological disorders, or symptomatic controls were included. sGFAP levels were measured using the SIMOA GFAP Advantage PLUS Kit (Quanterix) and the Duplex RUO Kit (GFAP/UCH-L1) (VEUDx, EZDiatech). Method comparison included Spearman correlation, Passing–Bablok regression, and Bland–Altman analysis. Outliers were removed using Tukey's IQR rule.
Results
Fifty-six patients (78.6 % women) were included. SIMOA reported markedly higher sGFAP concentrations (median 110.5 ng/L, IQR 83.2–176) compared with VEUS (median 6.13 ng/L, IQR 3.88–6.87). No significant correlation was observed between platforms (r = 0.02, p = 0.89). Passing–Bablok regression demonstrated a near-zero slope, indicating absent linear association. Bland–Altman analysis showed proportional bias, with VEUS measuring on average 21 % of SIMOA values and increasing divergence at higher concentrations.
Conclusion
These results do not support substituting sGFAP measurements between VEUS and SIMOA assays.
血清胶质原纤维酸性蛋白（sGFAP）作为星形胶质细胞损伤的生物标志物被越来越多地研究，但超灵敏分析平台之间的比较数据有限。本研究评估了新开发的VEUS技术与已建立的单分子阵列（SIMOA）方法之间的一致性。方法：在俄斯特拉发大学医院神经内科进行单中心回顾性分析。患者≥18年复发缓解型多发性硬化症，非炎症性神经系统疾病，或症状对照。使用SIMOA GFAP Advantage PLUS Kit （Quanterix）和Duplex RUO Kit (GFAP/UCH-L1) （VEUDx, EZDiatech）测量sGFAP水平。方法比较采用Spearman相关、Passing-Bablok回归、Bland-Altman分析。使用Tukey的IQR规则去除异常值。结果：共纳入56例患者（78.6%为女性）。SIMOA报告的sGFAP浓度（中位数为110.5 ng/L， IQR为83.2-176）明显高于VEUS（中位数为6.13 ng/L， IQR为3.88-6.87）。平台间无显著相关性（r = 0.02, p = 0.89）。passingbablok回归显示斜率接近于零，表明不存在线性关联。Bland-Altman分析显示出比例偏差，VEUS平均测量SIMOA值的21%，且浓度越高，差异越大。结论：这些结果不支持在VEUS和SIMOA测定之间替代sGFAP测定。
{"title":"Comparison of SIMOA and VEUS technologies for serum glial fibrillary acidic protein measurement","authors":"Radovan Bunganic , Kamila Zondra Revendova , Pavel Hradilek , Pavlina Kusnierova","doi":"10.1016/j.jneuroim.2025.578825","DOIUrl":"10.1016/j.jneuroim.2025.578825","url":null,"abstract":"<div><h3>Introduction</h3><div>Serum glial fibrillary acidic protein (sGFAP) is increasingly studied as a biomarker of astroglial injury, but comparative data between ultra-sensitive analytical platforms are limited. This study evaluated the agreement between the newly developed VEUS technology and the established single-molecule array (SIMOA) method.</div></div><div><h3>Methods</h3><div>A single-centre retrospective analysis was conducted at the Department of Neurology, University Hospital Ostrava. Patients ≥18 years with relapsing-remitting multiple sclerosis, non-inflammatory neurological disorders, or symptomatic controls were included. sGFAP levels were measured using the SIMOA GFAP Advantage PLUS Kit (Quanterix) and the Duplex RUO Kit (GFAP/UCH-L1) (VEUDx, EZDiatech). Method comparison included Spearman correlation, Passing–Bablok regression, and Bland–Altman analysis. Outliers were removed using Tukey's IQR rule.</div></div><div><h3>Results</h3><div>Fifty-six patients (78.6 % women) were included. SIMOA reported markedly higher sGFAP concentrations (median 110.5 ng/L, IQR 83.2–176) compared with VEUS (median 6.13 ng/L, IQR 3.88–6.87). No significant correlation was observed between platforms (<em>r</em> = 0.02, <em>p</em> = 0.89). Passing–Bablok regression demonstrated a near-zero slope, indicating absent linear association. Bland–Altman analysis showed proportional bias, with VEUS measuring on average 21 % of SIMOA values and increasing divergence at higher concentrations.</div></div><div><h3>Conclusion</h3><div>These results do not support substituting sGFAP measurements between VEUS and SIMOA assays.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578825"},"PeriodicalIF":2.5,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-28DOI: 10.1016/j.jneuroim.2025.578823
Nicola Salvatore Orefice , Roberta Amoriello , Olfa Maghrebi , Chiara Ballerini , Giovanni Baldi , Roberta Arpino , Marianna Abate , Silvia Zappavigna , Luisa Pastò , Maria Pia Amato , Michele Caraglia , Clara Ballerini
Introduction
Multiple Sclerosis (MS) is an autoimmune, demyelinating, inflammatory disorder. The anti-CD20 monoclonal antibody ocrelizumab targets B cells, effectively controlling the disease. MicroRNAs (miRNAs), small molecules modulating immune responses and neuroinflammation, may serve as biomarkers for disease progression, though the impact of anti-CD20 remains unclear. We hereby selected three miRNAs of interest for their relevance in experimental autoimmune encephalomyelitis (EAE) and MS, miR-124a-3p, miR-125b-5p, and miR-223-3p.
Methods
We examined these miRNAs in the spinal cord of EAE mice treated with a nanoformulation of anti-CD20 and in 23 MS patients' serum (19 relapsing-remitting [RR] and 4 primary-progressive [PP]) before (T0) and after six months (T6) of ocrelizumab, alongside with serum cytokines and chemokines.
Results
We found reduced (*p = 0.045) miR-223-3p in nano-anti-CD20-treated mice and in patients (*p = 0.030) with inactive MS. RRMS showed varying miRNA expression, while PPMS exhibited reduced (*p = 0.029) miR-124a-3p at T6. CXCL10 was elevated (*p = 0.024) in patients with active MS. Overall, six cytokines increased at T6, with interleukin 6 (IL6) negatively correlating with miR-223-3p. Gene analysis showed that IL6 gene is among miRNAs' targets, alongside inflammatory pathways.
Conclusions
This is the first study to compare miR-124a-3p, miR-125b-5p, and miR-223-3p in both EAE and MS patients undergoing anti-CD20 therapy, suggesting subtype-specific molecular responses, identifying miR-223-3p as a potential biomarker of treatment response, and highlighting immune regulatory pathways as key mechanisms linking these miRNAs to disease progression and therapy outcomes.
{"title":"Early response in cytokine and miR-124a, -125b, -223 expression to anti-CD20 in Multiple Sclerosis and its animal model – a preliminary analysis","authors":"Nicola Salvatore Orefice , Roberta Amoriello , Olfa Maghrebi , Chiara Ballerini , Giovanni Baldi , Roberta Arpino , Marianna Abate , Silvia Zappavigna , Luisa Pastò , Maria Pia Amato , Michele Caraglia , Clara Ballerini","doi":"10.1016/j.jneuroim.2025.578823","DOIUrl":"10.1016/j.jneuroim.2025.578823","url":null,"abstract":"<div><h3>Introduction</h3><div>Multiple Sclerosis (MS) is an autoimmune, demyelinating, inflammatory disorder. The anti-CD20 monoclonal antibody ocrelizumab targets B cells, effectively controlling the disease. MicroRNAs (miRNAs), small molecules modulating immune responses and neuroinflammation, may serve as biomarkers for disease progression, though the impact of anti-CD20 remains unclear. We hereby selected three miRNAs of interest for their relevance in experimental autoimmune encephalomyelitis (EAE) and MS, miR-124a-3p, miR-125b-5p, and miR-223-3p.</div></div><div><h3>Methods</h3><div>We examined these miRNAs in the spinal cord of EAE mice treated with a nanoformulation of anti-CD20 and in 23 MS patients' serum (19 relapsing-remitting [RR] and 4 primary-progressive [PP]) before (T0) and after six months (T6) of ocrelizumab, alongside with serum cytokines and chemokines.</div></div><div><h3>Results</h3><div>We found reduced (*<em>p</em> = 0.045) miR-223-3p in nano-anti-CD20-treated mice and in patients (*<em>p</em> = 0.030) with inactive MS. RRMS showed varying miRNA expression, while PPMS exhibited reduced (*<em>p</em> = 0.029) miR-124a-3p at T6. CXCL10 was elevated (*<em>p</em> = 0.024) in patients with active MS. Overall, six cytokines increased at T6, with interleukin 6 (IL6) negatively correlating with miR-223-3p. Gene analysis showed that IL6 gene is among miRNAs' targets, alongside inflammatory pathways.</div></div><div><h3>Conclusions</h3><div>This is the first study to compare miR-124a-3p, miR-125b-5p, and miR-223-3p in both EAE and MS patients undergoing anti-CD20 therapy, suggesting subtype-specific molecular responses, identifying miR-223-3p as a potential biomarker of treatment response, and highlighting immune regulatory pathways as key mechanisms linking these miRNAs to disease progression and therapy outcomes.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578823"},"PeriodicalIF":2.5,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145677888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-28DOI: 10.1016/j.jneuroim.2025.578803
Masatoshi Hayashi
Myasthenia gravis (MG) is a signaling disorder caused by immune abnormalities at the neuromuscular junction, resulting in symptoms such as muscle weakness and fatigue. Groundbreaking research since the 1970s has revealed the pathophysiology of this disease to be a T cell-dependent, B cell-associated antibody-producing disease. Half a century ago, many patients died of the disease, Today, the mortality rate has declined with many patients achieving remission. Here, I review MG pathophysiology, issues in treatment considerations specific to childhood and adolescence, and examine how racial, cultural, and geographic differences impact the clinical phenotype and treatment practices in childhood-onset MG across East Asia and Western Europe.
{"title":"Diversity of childhood-onset myasthenia gravis: pathophysiology and treatment","authors":"Masatoshi Hayashi","doi":"10.1016/j.jneuroim.2025.578803","DOIUrl":"10.1016/j.jneuroim.2025.578803","url":null,"abstract":"<div><div>Myasthenia gravis (MG) is a signaling disorder caused by immune abnormalities at the neuromuscular junction, resulting in symptoms such as muscle weakness and fatigue. Groundbreaking research since the 1970s has revealed the pathophysiology of this disease to be a T cell-dependent, B cell-associated antibody-producing disease. Half a century ago, many patients died of the disease, Today, the mortality rate has declined with many patients achieving remission. Here, I review MG pathophysiology, issues in treatment considerations specific to childhood and adolescence, and examine how racial, cultural, and geographic differences impact the clinical phenotype and treatment practices in childhood-onset MG across East Asia and Western Europe.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578803"},"PeriodicalIF":2.5,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145617639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-28DOI: 10.1016/j.jneuroim.2025.578824
Parth Aphale, Himanshu Shekhar, Shashank Dokania
{"title":"The need for functional correlation in assessing peripheral and CNS immunity during EBV reactivation","authors":"Parth Aphale, Himanshu Shekhar, Shashank Dokania","doi":"10.1016/j.jneuroim.2025.578824","DOIUrl":"10.1016/j.jneuroim.2025.578824","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578824"},"PeriodicalIF":2.5,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-25DOI: 10.1016/j.jneuroim.2025.578821
Merna Wagdy , Abeer A. Ibrahim , Alaa M. Yahia, Rola M. Maher, Afaf Hany Abo-Elwafa, Alyaa Salah, Yasmin M. Heikal
Alzheimer's disease (AD) is a progressive neurodegenerative disorder identified by cognitive decline, memory loss, and behavioral changes, affecting approximately 50 million people worldwide. Genetic predisposition, environmental variables, and aging all play a role in the development of AD. Current therapeutic approaches primarily focus on alleviating symptoms through drugs such as donepezil and memantine. However, these treatments offer limited efficacy and may be accompanied by adverse effects. In contrast, natural therapies derived from algae present a promising alternative. Microalgae, including Chlorella and Spirulina, and macroalgae such as Fucus vesiculosus, Ecklonia cava, Sargassum, Laminaria japonica, and Fucus species, are rich in bioactive molecules having antioxidant and anti-inflammatory characteristics. These substances demonstrated potential in addressing the pathological features of AD, such as oxidative stress and neuroinflammation. Furthermore, advances in biotechnological tools like CRISPR-Cas9 gene editing are poised to enhance the efficacy of these natural therapies by targeting and modifying disease-associated genes. This review aims to bridge the fields of neurobiotechnology and marine bioresources by examining the synergistic potential of algal compounds and gene-editing strategies in combating Alzheimer's disease. Algal-derived compounds are utilized in pharmaceuticals, nutraceuticals, and dietary supplements, and may offer neuroprotective benefits that could aid in the prevention or treatment of AD.By integrating insights from molecular biology, pharmacology, and genomics, we seek to illuminate a novel, multidisciplinary framework for future therapeutic innovation.
{"title":"Neurobiotech innovative strategies targeting Alzheimer's disease through therapeutic micro and macroalgae potentials","authors":"Merna Wagdy , Abeer A. Ibrahim , Alaa M. Yahia, Rola M. Maher, Afaf Hany Abo-Elwafa, Alyaa Salah, Yasmin M. Heikal","doi":"10.1016/j.jneuroim.2025.578821","DOIUrl":"10.1016/j.jneuroim.2025.578821","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a progressive neurodegenerative disorder identified by cognitive decline, memory loss, and behavioral changes, affecting approximately 50 million people worldwide. Genetic predisposition, environmental variables, and aging all play a role in the development of AD. Current therapeutic approaches primarily focus on alleviating symptoms through drugs such as donepezil and memantine. However, these treatments offer limited efficacy and may be accompanied by adverse effects. In contrast, natural therapies derived from algae present a promising alternative. Microalgae, including Chlorella and Spirulina, and macroalgae such as <em>Fucus vesiculosus</em>, <em>Ecklonia cava</em>, Sargassum, <em>Laminaria japonica</em>, and Fucus species, are rich in bioactive molecules having antioxidant and anti-inflammatory characteristics. These substances demonstrated potential in addressing the pathological features of AD, such as oxidative stress and neuroinflammation. Furthermore, advances in biotechnological tools like CRISPR-Cas9 gene editing are poised to enhance the efficacy of these natural therapies by targeting and modifying disease-associated genes. This review aims to bridge the fields of neurobiotechnology and marine bioresources by examining the synergistic potential of algal compounds and gene-editing strategies in combating Alzheimer's disease. Algal-derived compounds are utilized in pharmaceuticals, nutraceuticals, and dietary supplements, and may offer neuroprotective benefits that could aid in the prevention or treatment of AD.By integrating insights from molecular biology, pharmacology, and genomics, we seek to illuminate a novel, multidisciplinary framework for future therapeutic innovation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578821"},"PeriodicalIF":2.5,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-23DOI: 10.1016/j.jneuroim.2025.578815
Vera Fominykh , Irina Kovaleva , Ekaterina Aksenova , Elena Kondrasheva , Narine Arzumanian , Dmitrii Averchenkov , Sergey Lapin , Vladimir Nazarov , Anna Moshnikova , Mikhail Levin , Alena Prusova , Larisa Burygina , Lev Brylev , Angelina Khannanova
Background
Autoimmune encephalitis (AE) comprises a group of immune-mediated central nervous system disorders and can present with psychiatric symptoms. This study aimed to prospectively identify and characterize the AE group in first psychotic episode (FEP) at the tertiary psychiatric hospital using clinical and instrumental data in combination with modified algorithm for AE in FEP; and retrospectively evaluate current diagnostic algorithms for AE and autoimmune psychosis (AP) based on obtained empirical data.
Methodology
We consecutively assessed all FEP patients admitted to psychiatric hospital according to inclusion-exclusion criteria. In all included patient's clinical picture was assessed, serum and cerebrospinal fluid (CSF) were taken at the acute stage of disorders. CSF oligoclonal bands, cytosis and protein level were tested in all CSF samples. Serum antineuronal antibodies (Abs) to intracellular antigens, NMDA, CASPR2, LGi1, GABAb, AMPA1,2, GAD Abs, thyroid serology, ANA, dsDNA Abs were measured. After the warning signs assessment, the second set of analyses were performed in patients with “red flags” and/or positive laboratory tests: CSF antineuronal antibodies (NMDA, CASPR2, LGi1, GABAb, AMPA1,2, GAD Abs), brain MRI, and oncological screening. AE diagnosis was made by Graus criteria. Immunosuppressive treatment was used in AE patients. We assessed the outcome after the treatment, and for all patients after 9–12 months follow-up.
Results
784 consecutive patients underwent the screening procedure as patients referred to the tertiary psychiatric hospital with FEP. After the inclusion/exclusion procedure, 143 patients were included in the study. We confirmed AE diagnosis in 5 patients (3.5 % of included patients): anti-AMPH, anti-AMPA 2, anti-GABAb, anti-yo AE, and AE with CSF antineuronal antibodies. 1 out of 5 patients died in the acute stage, 3 have good outcomes and return to work.
Conclusion
We revealed 3.5 % AE in the FEP cohort in an East-European tertiary psychiatric hospital. No clinical “red flags” were detected in 1 patient. In 1 patient Ab was detected only in CSF. AE criteria + “red flags” assessment help to reveal 4 out 5 cases. 1 case was found at serum screening and confirmed by CSF analysis. Our results supported the necessity of valid “red flags” panel, serum and CSF antibody testing in the FEP cohort at admission for improving AE diagnostics in FEP.
{"title":"Autoimmune encephalitis in first episode psychosis: Prospective non-interventional longitudinal study in tertiary psychiatric center","authors":"Vera Fominykh , Irina Kovaleva , Ekaterina Aksenova , Elena Kondrasheva , Narine Arzumanian , Dmitrii Averchenkov , Sergey Lapin , Vladimir Nazarov , Anna Moshnikova , Mikhail Levin , Alena Prusova , Larisa Burygina , Lev Brylev , Angelina Khannanova","doi":"10.1016/j.jneuroim.2025.578815","DOIUrl":"10.1016/j.jneuroim.2025.578815","url":null,"abstract":"<div><h3>Background</h3><div>Autoimmune encephalitis (AE) comprises a group of immune-mediated central nervous system disorders and can present with psychiatric symptoms. This study aimed to prospectively identify and characterize the AE group in first psychotic episode (FEP) at the tertiary psychiatric hospital using clinical and instrumental data in combination with modified algorithm for AE in FEP; and retrospectively evaluate current diagnostic algorithms for AE and autoimmune psychosis (AP) based on obtained empirical data.</div></div><div><h3>Methodology</h3><div>We consecutively assessed all FEP patients admitted to psychiatric hospital according to inclusion-exclusion criteria. In all included patient's clinical picture was assessed, serum and cerebrospinal fluid (CSF) were taken at the acute stage of disorders. CSF oligoclonal bands, cytosis and protein level were tested in all CSF samples. Serum antineuronal antibodies (Abs) to intracellular antigens, NMDA, CASPR2, LGi1, GABAb, AMPA1,2, GAD Abs, thyroid serology, ANA, dsDNA Abs were measured. After the warning signs assessment, the second set of analyses were performed in patients with “red flags” and/or positive laboratory tests: CSF antineuronal antibodies (NMDA, CASPR2, LGi1, GABAb, AMPA1,2, GAD Abs), brain MRI, and oncological screening. AE diagnosis was made by Graus criteria. Immunosuppressive treatment was used in AE patients. We assessed the outcome after the treatment, and for all patients after 9–12 months follow-up.</div></div><div><h3>Results</h3><div>784 consecutive patients underwent the screening procedure as patients referred to the tertiary psychiatric hospital with FEP. After the inclusion/exclusion procedure, 143 patients were included in the study. We confirmed AE diagnosis in 5 patients (3.5 % of included patients): anti-AMPH, anti-AMPA 2, anti-GABAb, anti-yo AE, and AE with CSF antineuronal antibodies. 1 out of 5 patients died in the acute stage, 3 have good outcomes and return to work.</div></div><div><h3>Conclusion</h3><div>We revealed 3.5 % AE in the FEP cohort in an East-European tertiary psychiatric hospital. No clinical “red flags” were detected in 1 patient. In 1 patient Ab was detected only in CSF. AE criteria + “red flags” assessment help to reveal 4 out 5 cases. 1 case was found at serum screening and confirmed by CSF analysis. Our results supported the necessity of valid “red flags” panel, serum and CSF antibody testing in the FEP cohort at admission for improving AE diagnostics in FEP.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578815"},"PeriodicalIF":2.5,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-23DOI: 10.1016/j.jneuroim.2025.578817
Vinícius Boldrini , Edgar Carnero Contentti
According to the 2025 IPND consensus, live cell-based assays (live CBA) are now established as the reference standard for screening AQP4-IgG autoantibodies in patients suspected of having AQP4-IgG-positive Neuromyelitis optica spectrum (NMOSD). However, resource-limited settings in Latin America (LATAM), where even commercial kits (fixed CBA) can be scarce, face significant difficulties in accessing local live CBA due to its higher implementation cost, the time required for experimentation, and its technical complexity.
In this narrative review, we identified 85 published studies that provide evidence of CBA locally used in LATAM countries. We identified 18 studies (21.1%) that used “live CBA” as the exclusive AQP4-IgG testing method. Brazil was the only country that had participated in all these reports. Argentina (n = 2, 2.3%), Mexico (n = 1, 1.1%), and Colombia (n = 1, 1.1%) have participated in studies combining “live CBA and fixed CBA”. Our literature review suggests that live CBA availability is approximately 20% when considered as a single testing method, or up to 27.1% (n = 23) when used to varying degrees in conjunction with fixed CBA. Notably, several studies (n = 37, 43.5%) we analyzed relied solely on commercial fixed assays for AQP4-IgG testing. Worryingly, nearly one-third (n = 25, 29.4%) of the studies we analyzed still use commercial kits in combination with other non‑gold-standard methods to detect AQP4-IgG. In general, fixed CBA was the most sensitive method in 62 studies (72.9%) from LATAM.
Based on our findings, here, we critically discuss the pressing need for live CBA dissemination across LATAM countries. This initiative will lead to more accurate epidemiological data, enable faster diagnosis, and improve access to highly effective therapies for AQP4-IgG-positive NMOSD patients living in this part of the world.
{"title":"Limited availability of live CBA for AQP4-IgG testing and its consequences for the diagnosis and treatment of NMOSD in Latin American countries","authors":"Vinícius Boldrini , Edgar Carnero Contentti","doi":"10.1016/j.jneuroim.2025.578817","DOIUrl":"10.1016/j.jneuroim.2025.578817","url":null,"abstract":"<div><div>According to the 2025 IPND consensus, live cell-based assays (<em>live CBA</em>) are now established as the reference standard for screening AQP4-IgG autoantibodies in patients suspected of having AQP4-IgG-positive Neuromyelitis optica spectrum (NMOSD). However, resource-limited settings in Latin America (LATAM), where even commercial kits (<em>fixed CBA</em>) can be scarce, face significant difficulties in accessing local <em>live CBA</em> due to its higher implementation cost, the time required for experimentation, and its technical complexity.</div><div>In this narrative review, we identified 85 published studies that provide evidence of CBA locally used in LATAM countries. We identified 18 studies (21.1%) that used “<em>live CBA”</em> as the exclusive AQP4-IgG testing method. Brazil was the only country that had participated in all these reports. Argentina (<em>n</em> = 2, 2.3%), Mexico (<em>n</em> = 1, 1.1%), and Colombia (<em>n</em> = 1, 1.1%) have participated in studies combining “<em>live CBA and fixed CBA</em>”. Our literature review suggests that <em>live CBA</em> availability is approximately 20% when considered as a single testing method, or up to 27.1% (<em>n</em> = 23) when used to varying degrees in conjunction with <em>fixed CBA.</em> Notably, several studies (<em>n</em> = 37, 43.5%) we analyzed relied solely on commercial fixed assays for AQP4-IgG testing. Worryingly, nearly one-third (<em>n</em> = 25, 29.4%) of the studies we analyzed still use commercial kits in combination with other non‑gold-standard methods to detect AQP4-IgG. In general, <em>fixed CBA</em> was the most sensitive method in 62 studies (72.9%) from LATAM.</div><div>Based on our findings, here, we critically discuss the pressing need for <em>live CBA</em> dissemination across LATAM countries. This initiative will lead to more accurate epidemiological data, enable faster diagnosis, and improve access to highly effective therapies for AQP4-IgG-positive NMOSD patients living in this part of the world.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578817"},"PeriodicalIF":2.5,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Physiological monitoring may be useful for monitoring the progression of MS and its underlying neurodegenerative processes
Objective
This cross-sectional study evaluated the feasibility of assessing associations of physiological parameters measured by a wearable sensor with CNS atrophy and lesion burden in individuals with MS.
Methods
Thirty MS patients (relapsing-remitting [n = 23], secondary progressive [n = 5], primary progressive [n = 2]) were monitored using a wrist-worn sensor (Fitbit inspire 3) for up to 30 days, and 29 physiological parameters were obtained. Global and regional brain volumes, T2 lesion volume (T2LV), and C2/3 cervical spinal cord cross-sectional area (C2/3 CSA) were analyzed based on brain MRI. Associations between sensor-derived parameters and neuroimaging measures were assessed using correlation analyses adjusted for age and gender
Results
The proportion of deep sleep was associated with T2LV (partial spearman's ρ [ρpartial] = −0.46, 95 % confidence interval [−0.74, −0.04]) and C2/3 CSA (ρpartial = 0.59 [0.32, 0.76]). The coefficient of variation of RR intervals during sleep was associated with normalized brain volume (ρpartial = 0.41 [0.00, 0.74]). The minimum (ρpartial = −0.44 [−0.72, −0.04]) and range of heart rate (ρpartial = 0.41 [0.08, 0.68]) during daytime, step counts (ρpartial = 0.64 [0.40, 0.82]), and total metabolic equivalents (ρpartial = 0.54 [0.18, 0.79]) were associated with C2/3 CSA
Conclusion
The findings suggest the feasibility of using wearable sensors to detect physiological parameters reflective of neuropathology in patients with MS.
{"title":"Wearable-based physiological monitoring and brain magnetic resonance imaging metrics in multiple sclerosis: A feasibility study","authors":"Yusei Miyazaki , Hiroaki Yokote , Juichi Fujimori , Kenzo Sakurai , Akifumi Hagiwara , Satoshi Fujino , Toshikazu Fukami , Eri Takahashi , Mai Miyagishi , Megumi Uwatoko , Yoko Sugimura , Itaru Amino , Sachiko Akimoto , Keisuke Izumi , Kazumichi Minato , Naoya Minami , Masaaki Niino","doi":"10.1016/j.jneuroim.2025.578819","DOIUrl":"10.1016/j.jneuroim.2025.578819","url":null,"abstract":"<div><h3><strong>Background</strong></h3><div>Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Physiological monitoring may be useful for monitoring the progression of MS and its underlying neurodegenerative processes</div></div><div><h3><strong>Objective</strong></h3><div>This cross-sectional study evaluated the feasibility of assessing associations of physiological parameters measured by a wearable sensor with CNS atrophy and lesion burden in individuals with MS.</div></div><div><h3><strong>Methods</strong></h3><div>Thirty MS patients (relapsing-remitting [<em>n</em> = 23], secondary progressive [<em>n</em> = 5], primary progressive [n = 2]) were monitored using a wrist-worn sensor (Fitbit inspire 3) for up to 30 days, and 29 physiological parameters were obtained. Global and regional brain volumes, T2 lesion volume (T2LV), and C2/3 cervical spinal cord cross-sectional area (C2/3 CSA) were analyzed based on brain MRI. Associations between sensor-derived parameters and neuroimaging measures were assessed using correlation analyses adjusted for age and gender</div></div><div><h3><strong>Results</strong></h3><div>The proportion of deep sleep was associated with T2LV (partial spearman's ρ [ρ<sub>partial</sub>] = −0.46, 95 % confidence interval [−0.74, −0.04]) and C2/3 CSA (ρ<sub>partial</sub> = 0.59 [0.32, 0.76]). The coefficient of variation of RR intervals during sleep was associated with normalized brain volume (ρ<sub>partial</sub> = 0.41 [0.00, 0.74]). The minimum (ρ<sub>partial</sub> = −0.44 [−0.72, −0.04]) and range of heart rate (ρ<sub>partial</sub> = 0.41 [0.08, 0.68]) during daytime, step counts (ρ<sub>partial</sub> = 0.64 [0.40, 0.82]), and total metabolic equivalents (ρ<sub>partial</sub> = 0.54 [0.18, 0.79]) were associated with C2/3 CSA</div></div><div><h3><strong>Conclusion</strong></h3><div>The findings suggest the feasibility of using wearable sensors to detect physiological parameters reflective of neuropathology in patients with MS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578819"},"PeriodicalIF":2.5,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-21DOI: 10.1016/j.jneuroim.2025.578818
Emanuela Bezerra dos Santos Ribeiro , Luiza dos Santos Heringer , Bruna dos Santos Ramalho , Tiago Bastos Taboada , Fernanda Martins de Almeida , Ana Maria Blanco Martinez
Spinal cord injury (SCI) occurs either after a sudden trauma or through a chronic process at segmental levels of the spinal cord, leading to potentially deleterious neural consequences for the central nervous system (CNS) due to the death of neurons, oligodendrocytes, and astrocytes, as well as significant losses in motor, sensory, and autonomic functions. After SCI, an inflammatory response occurs, with cells such as macrophages and microglia being recruited. These cells are responsible for removing damaged tissue and secreting pro-inflammatory and anti-inflammatory cytokines and chemokines. Additionally, a protein called galectin-3 has been described as participating in cell activation, proliferation, and migration, acting as a mediator of inflammation in neurodegeneration. Thus, different populations of inflammatory cells in the injured nervous parenchyma can be characterized. In this study, we used a spinal cord contusion-compression model in wild-type C57Bl/6 mice (WT) and galectin-3 knockout mice (GAL3−/−) to histologically characterize the lesion, focusing on astrocyte, macrophage, and microglial populations. Our results showed a significant reduction in lesion propagation in GAL3−/− animals compared to WT animals. Moreover, GAL3−/− animals exhibited reduced astrogliosis compared to WT animals. Immunohistochemistry revealed that GAL3−/− animals had a larger area marked for the anti-inflammatory marker Arginase-1 and a smaller area marked for the pro-inflammatory marker iNOS compared to WT animals. We conclude that galectin-3 plays a critical role in the inflammatory process following spinal cord injury, and its absence may contribute to reduced lesion progression, decreased astrogliosis, and the promotion of an inflammatory response with a more anti-inflammatory profile.
Significance statement
This study highlights galectin-3 as a central mediator of the inflammatory response after spinal cord injury, demonstrating that galectin-3 deficiency limits lesion progression, attenuates astrogliosis, and promotes an anti-inflammatory profile. Thus, galectin-3 may represent a promising potential therapeutic target for clinical applications in neurodegenerative diseases.
{"title":"Modulation of inflammatory and regenerative responses by Galectin-3 after spinal cord injury in wild-type and Galectin-3 knockout mice","authors":"Emanuela Bezerra dos Santos Ribeiro , Luiza dos Santos Heringer , Bruna dos Santos Ramalho , Tiago Bastos Taboada , Fernanda Martins de Almeida , Ana Maria Blanco Martinez","doi":"10.1016/j.jneuroim.2025.578818","DOIUrl":"10.1016/j.jneuroim.2025.578818","url":null,"abstract":"<div><div>Spinal cord injury (SCI) occurs either after a sudden trauma or through a chronic process at segmental levels of the spinal cord, leading to potentially deleterious neural consequences for the central nervous system (CNS) due to the death of neurons, oligodendrocytes, and astrocytes, as well as significant losses in motor, sensory, and autonomic functions. After SCI, an inflammatory response occurs, with cells such as macrophages and microglia being recruited. These cells are responsible for removing damaged tissue and secreting pro-inflammatory and anti-inflammatory cytokines and chemokines. Additionally, a protein called galectin-3 has been described as participating in cell activation, proliferation, and migration, acting as a mediator of inflammation in neurodegeneration. Thus, different populations of inflammatory cells in the injured nervous parenchyma can be characterized. In this study, we used a spinal cord contusion-compression model in wild-type C57Bl/6 mice (WT) and galectin-3 knockout mice (GAL3−/−) to histologically characterize the lesion, focusing on astrocyte, macrophage, and microglial populations. Our results showed a significant reduction in lesion propagation in GAL3−/− animals compared to WT animals. Moreover, GAL3−/− animals exhibited reduced astrogliosis compared to WT animals. Immunohistochemistry revealed that GAL3−/− animals had a larger area marked for the anti-inflammatory marker Arginase-1 and a smaller area marked for the pro-inflammatory marker iNOS compared to WT animals. We conclude that galectin-3 plays a critical role in the inflammatory process following spinal cord injury, and its absence may contribute to reduced lesion progression, decreased astrogliosis, and the promotion of an inflammatory response with a more anti-inflammatory profile.</div></div><div><h3>Significance statement</h3><div>This study highlights galectin-3 as a central mediator of the inflammatory response after spinal cord injury, demonstrating that galectin-3 deficiency limits lesion progression, attenuates astrogliosis, and promotes an anti-inflammatory profile. Thus, galectin-3 may represent a promising potential therapeutic target for clinical applications in neurodegenerative diseases.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578818"},"PeriodicalIF":2.5,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145587881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-21DOI: 10.1016/j.jneuroim.2025.578820
Christian Messina
{"title":"IL-17 and IL-22 in Guillain-Barré syndrome: Untangling disease-specific signals from confounding factors","authors":"Christian Messina","doi":"10.1016/j.jneuroim.2025.578820","DOIUrl":"10.1016/j.jneuroim.2025.578820","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578820"},"PeriodicalIF":2.5,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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