Neurology® Neuroimmunology & Neuroinflammation最新文献

{"title":"Contribution of Blood Biomarkers to Multiple Sclerosis Diagnosis.","authors":"Manuel Comabella, Agustín Pappolla, Enric Monreal, Nicolás Fissolo, Augusto Cesaar Sao-Avilés, Georgina Arrambide, Pere Carbonell-Mirabent, Lucía Gutierrez, Álvaro Cobo-Calvo, Carmen Tur, Javier Villacieros-Álvarez, Ángela Vidal-Jordana, Joaquín Castilló, Ingrid Galán, Mercedes Espiño, Helena Ariño, Luca Bollo, Marta Rodríguez Barranco, Luciana Soledad Midaglia, René Carvajal, Noelia Villarrubia, José Ignacio Fernández Velasco, Breogán Rodríguez Acevedo, Lucienne F Costa Frossard, Andreu Vilaseca, Cristina Auger, Ana Zabalza, Susana Sainz De La Maza, Neus Mongay-Ochoa, Jordi Río, Jaume Sastre-Garriga, Àlex Rovira, Mar Tintoré, Luisa M Villar, Xavier Montalban","doi":"10.1212/NXI.0000000000200370","DOIUrl":"10.1212/NXI.0000000000200370","url":null,"abstract":"<p><strong>Background and objectives: </strong>Invasive procedures may delay the diagnostic process in multiple sclerosis (MS). We investigated the added value of serum neurofilament light chain (sNfL), glial fibrillary acidic protein (sGFAP), chitinase-3-like 1 (sCHI3L1), and the immune responses to the Epstein-Barr virus-encoded nuclear antigen 1 to current MS diagnostic criteria.</p><p><strong>Methods: </strong>In this multicentric study, we selected patients from 2 prospective cohorts presenting a clinically isolated syndrome (CIS). Patients were classified as (1) not presenting dissemination in space (DIS) nor dissemination in time (DIT) (noDIS and noDIT); (2) presenting DIS without DIT (DIS and noDIT); and (3) presenting both (DIS and DIT), which were used as a reference. sNfL, sGFAP, and sCHI3L1 levels were measured with single-molecule array immunoassays and EBNA1-specific IgG levels with ELISA. Biomarker levels were compared between groups using linear regression models. Receiver operating characteristic curve analyses and Youden Index were used to determine cutoff values associated with MS diagnosis during follow-up.</p><p><strong>Results: </strong>We included 181 patients (66.3% females, mean [SD] age of 35.0 [9.7] years). At baseline, 25 (13.8%) were classified as noDIS and noDIT, 62 (34.3%) as DIS and noDIT, and 94 (51.9%) as DIS and DIT. Only sNfL Z-scores discriminated between groups (DIS and DIT vs DIS and noDIT [<i>p</i> = 0.002], DIS and DIT vs noDIS and noDIT [<i>p</i> < 0.001], and DIS and noDIT vs noDIS and noDIT [<i>p</i> = 0.026]). In noDIS and noDIT patients (median interquartile range [IQR] follow-up of 8.1 [5.0-11.7] years), high sNfL Z-scores best predicted MS diagnosis (specificity [SP] and 95% CI of 93.3% [68.1-99.8] and positive predictive value [PPV] of 87.5% [47.3-99.7]). Among DIS and noDIT patients (median [IQR] follow-up of 6.8 [4.0-9.1] years), high sNfL Z-scores best predicted MS diagnosis (SP of 80% [28.4-99.5] and PPV of 97.3% [85.8-99.9]) without considering oligoclonal band (OB) status. In the subset of patients of this group with negative OBs, a combination of high sNfL Z-scores and sGFAP levels predicted MS diagnosis (SP of 100% [39.8-100] and PPV of 100% [54.1-100]).</p><p><strong>Discussion: </strong>These results suggest that sNfL and sGFAP may be incorporated in particular scenarios to diagnose MS in patients with CIS not fulfilling current diagnostic criteria.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200370"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant Complement Activation Is Associated With Structural Brain Damage in Multiple Sclerosis.","authors":"Johanna Oechtering, Sabine Anna Schaedelin, Kerstin Stein, Aleksandra Maleska Maceski, Lester Melie-Garcia, Pascal Benkert, Alessandro Cagol, Selina Leber, Riccardo Galbusera, Esther Ruberte, Wayne Hu, Ferhan Qureshi, Annette Orleth, Lilian Demuth, Eline Willemse, Ingmar Heijnen, Axel Regeniter, Tobias J Derfuss, Bettina Fischer-Barnicol, Lutz Achtnichts, Stefanie Mueller, Robert Hoepner, Patrice H Lalive, Claire Bridel, Marcus D'Souza, Caroline Pot, Renaud A Du Pasquier, Claudio Gobbi, Chiara Zecca, Heinz Wiendl, Johanna Maria Lieb, Christina Lamers, Ludwig Kappos, Marten Trendelenburg, David Leppert, Cristina Granziera, Jens Kuhle, Jan D Lünemann","doi":"10.1212/NXI.0000000000200361","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200361","url":null,"abstract":"<p><strong>Background and objectives: </strong>Levels of activated complement proteins in the CSF are increased in people with multiple sclerosis (MS) and are associated with clinical disease severity. In this study, we determined whether complement activation profiles track with quantitative MRI metrics and liquid biomarkers indicative of disease activity and progression.</p><p><strong>Methods: </strong>Complement components and activation products (Factor H and I, C1q, C3, C4, C5, Ba, Bb, C3a, C4a, C5a, and sC5b-9) and liquid biomarkers (neurofilament light chain, glial fibrillary acidic protein [GFAP], CXCL-13, CXCL-9, and IL-12b) were quantified in the CSF of 112 patients with clinically isolated syndromes and 127 patients with MS; longitudinal MRIs according to a standardized protocol of the Swiss MS cohort were assessed. We used multivariable models to analyze associations of the 12 complement parameters as individual independent variables and longitudinal brain volumes, T2-weighted (T2w) lesion volumes, contrast-enhancing (CELs) and paramagnetic rim lesions (PRLs), and molecular biomarkers as dependent variables, respectively.</p><p><strong>Results: </strong>Strongest associations with accelerated brain atrophy were found for C4a: doubling of C4a CSF levels was associated with an additional brain volume loss of -0.24% (95% CI -0.31% to -0.16%; <i>p</i> < 0.0001) per year, followed by Ba and C3a (-0.22% [-0.29% to -0.15%]) and -0.13% ([-0.21 to -0.06]; both <i>p</i> < 0.001). Doubling of C3a, Ba, and C4a levels correlated with 2.2- (1.6-3.0; <i>p</i> < 0.0001), 2.0- (1.3-3.1; <i>p</i> = 0.0038), and 1.8-fold (1.2-2.6; <i>p</i> = 0.0029) increased longitudinal T2w lesion volumes; C3a and Ba were associated with 2.5- (1.4-4.6; <i>p</i> = 0.0022) and 3.3-fold (1.5-7.2; <i>p</i> = 0.0024) higher odds for CELs and 2.6- (1.7-4.0; <i>p</i> < 0.0001) and 2.3-fold (1.3-4.3; <i>p</i> = 0.006) increased PRL incidence rates. C1q, C3a, and C4a were associated with higher GFAP levels, and CXCL-13, CXCL-9, and IL-12b analyses showed consistent patterns with strongest associations for C1q, followed by Ba, C3a, and C4a.</p><p><strong>Discussion: </strong>Intrathecal complement activation is consistently associated with MRI metrics and liquid biomarkers indicative for MS disease activity and progression. Our results demonstrate that aberrant complement activation is strongly associated with structural brain damage in MS. Therapeutic targeting of the complement system might limit disability accumulation due to MS.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200361"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Approaches to Treatment of Immune-Mediated Chronic Intestinal Pseudo-Obstruction.","authors":"Andreu Vilaseca, Paula Arranz, Arnau Llaurado, Ana Zabalza, Elianet Gisell Fonseca, Inmaculada Medina, Maria Amelia Gómez Lorente, Luis Alcalá-González, Natalia Borruel, José Luis Fernández-Forcelledo, Helena Ariño, Thais Armangue, Xavier Montalban, Francesc Graus, Carolina Malagelada","doi":"10.1212/NXI.0000000000200369","DOIUrl":"10.1212/NXI.0000000000200369","url":null,"abstract":"<p><strong>Background and objectives: </strong>The optimal immunosuppressive treatment for autoimmune chronic intestinal pseudo-obstruction (CIPO) is unknown due to lack of clinical trials. Even less data exist on treatment recommendations for patients who do not respond to first-line immunotherapy.</p><p><strong>Methods: </strong>We describe 4 patients with autoimmune CIPO treated with vedolizumab (3/4), a monoclonal antibody that interferes the lymphocyte trafficking to the gastrointestinal tract, or rituximab (1/4) who did not respond to steroids or IV immunoglobulins. We made a systematic review of previously published cases of CIPO treated with these biological agents.</p><p><strong>Results: </strong>Vedolizumab was effective in 2 of 3 patients but failed in a child with nonparaneoplastic anti-Hu-associated CIPO, who had generalized dysautonomia. The 2 patients who responded to vedolizumab had an isolated CIPO, and they did not present neuronal antibodies. Rituximab was prescribed in a case of anti-Hu-associated, nonparaneoplastic CIPO, who showed a complete clinical response after this treatment. Our review of the literature retrieved 4 previous cases of autoimmune CIPO treated with rituximab but none treated with vedolizumab. All patients treated with rituximab had Hu antibodies. Two patients showed a clinical response to the treatment with rituximab.</p><p><strong>Discussion: </strong>Our findings underscore the potential efficacy of rituximab and vedolizumab in the management of autoimmune CIPO refractory to first-line treatments.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200369"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11805607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mood Disorder and Multimorbidity Complicating a Multiple Sclerosis Diagnosis: From the National Multiple Sclerosis Society Case Conference Proceedings.","authors":"Jonathan D Krett, Claire Riley, Scott S Zamvil, Myla D Goldman, Scott D Newsome, Shiv Saidha","doi":"10.1212/NXI.0000000000200376","DOIUrl":"10.1212/NXI.0000000000200376","url":null,"abstract":"<p><p>A 28-year-old Black woman presented with both typical and atypical features of multiple sclerosis in the setting of multimorbidity including psychiatric history, complicating diagnosis and treatment. This case illustrates the importance of differential diagnosis and longitudinal follow-up before committing to disease-modifying therapy. Individualized treatment decision-making is highlighted.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200376"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11820807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple Sclerosis: A Virus-Induced Gliopathy?","authors":"Joseph J Sabatino, Lawrence Steinman","doi":"10.1212/NXI.0000000000200383","DOIUrl":"10.1212/NXI.0000000000200383","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200383"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11820804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Neurology® Neuroimmunology and Neuroinflammation</i> Enters Its Second Decade.","authors":"Scott S Zamvil","doi":"10.1212/NXI.0000000000200385","DOIUrl":"10.1212/NXI.0000000000200385","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200385"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11813232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluorescein Angiography as a Surrogate Marker of Disease Activity in Susac Syndrome.","authors":"Laura Guttieres, Lea Vannelli, Sarah Demortiere, Marine Perriguey, Maya Elziere, Pierre Durozard, Clemence Boutiere, Audrey Rico, Frederic Hilezian, Jan-Patrick Stellmann, Jean Pelletier, Adil Maarouf, Natacha Stolowy, Bertrand Audoin","doi":"10.1212/NXI.0000000000200379","DOIUrl":"10.1212/NXI.0000000000200379","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the sensitivity of fluorescein angiography (FA) in detecting disease activity in Susac syndrome.</p><p><strong>Methods: </strong>We conducted a blinded analysis of all FA, brain MRI, and audiogram examinations performed throughout the follow-up of patients with Susac syndrome.</p><p><strong>Results: </strong>A total of 79 FA examinations, 85 brain MRI scans, and 49 audiograms were analyzed from 9 patients followed for a mean (SD) period of 6 (4) years. Disease activity was detected in 41.5% of FA examinations, 10.5% of MRI scans, and 25% of audiograms (FA vs MRI, <i>p</i> < 0.0001; FA vs audiogram, <i>p</i> = 0.06; audiogram vs MRI, <i>p</i> < 0.05). Within 3 months of clinical relapses, activity was observed in 57%, 24%, and 27% of FA, MRI, and audiogram examinations, respectively (FA vs MRI, <i>p</i> < 0.05; FA vs audiogram, <i>p</i> = 0.09; audiogram vs MRI, <i>p</i> = 1). Quantitative analysis of FA showed a mean (SD) of 2.5 (2.5) leakages (both eyes) during relapses compared with 1.2 (1.4) during remission (<i>p</i> < 0.05).</p><p><strong>Discussion: </strong>FA, particularly arterial leakage, demonstrated the highest sensitivity in detecting disease activity and may be a valuable tool for treatment management in Susac syndrome. Future studies with larger samples should aim to identify the optimal threshold of FA changes associated with an increased risk of relapse.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200379"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11805606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of Autoimmune Encephalitis in a 7-Year-Old Child With CTLA-4 Haploinsufficiency and AMPA Receptor Antibodies: A Case Report.","authors":"Marjolijn S W Quaak, Michiel S J Buijze, Virginie J M Verhoeven, Clementien Vermont, Emilie P Buddingh, Maud Heredia, Janneke N Samsom, Maarten J Titulaer, Annemarie M C van Rossum, Sylvia Kamphuis, Rinze Frederik Neuteboom","doi":"10.1212/NXI.0000000000200381","DOIUrl":"10.1212/NXI.0000000000200381","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200381"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11825085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive Myelitis in a 63-Year-Old Woman: A Case Report From the National Multiple Sclerosis Society Case Conference Proceedings.","authors":"Kimberly A DiMauro, Morgan E Heber, Jonathan Lee, Jeffrey A Cohen, Eoin P Flanagan, Claire Riley, Myla D Goldman, Scott S Zamvil, Amy C Kunchok","doi":"10.1212/NXI.0000000000200382","DOIUrl":"10.1212/NXI.0000000000200382","url":null,"abstract":"<p><p>We present a case of myelitis in a 63-year-old woman with breast adenocarcinoma treated with pembrolizumab. MRI showed multiple T2-hyperintense lesions throughout the spinal cord, and CSF demonstrated lymphocytic pleocytosis. We discuss the differential diagnosis of myelitis in the setting of cancer and immune checkpoint inhibitors.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200382"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11813231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired Presynaptic Function Contributes Significantly to the Pathology of Glycine Receptor Autoantibodies.","authors":"Anna-Lena Wiessler, Fang Zheng, Christian Werner, Margarita Habib, Erdem Tuzun, Christian Alzheimer, Claudia Sommer, Carmen Villmann","doi":"10.1212/NXI.0000000000200364","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200364","url":null,"abstract":"<p><strong>Background and objectives: </strong>Autoantibodies (aAbs) against glycine receptors (GlyRs) are mainly associated with the rare neurologic diseases stiff person syndrome (SPS) and progressive encephalomyelitis with rigidity and myoclonus (PERM). GlyR aAbs are also found in other neurologic diseases such as epilepsy. The aAbs bind to different GlyR α-subunits and, more rarely, also to the GlyR β-subunit. So far, studies on the pathogenic effects of the aAbs have focused on postsynaptic, heteromeric GlyRs, reporting a loss of ion channel function and receptor internalization upon aAb binding. We asked whether the aAbs also affect expression and functionality of presynaptic homomeric GlyRs.</p><p><strong>Methods: </strong>We established interneuron cultures from mouse embryonic spinal cord neurons and used protein biochemistry and super-resolution microscopy to determine aAb binding to presynaptic GlyRs in a uniform neuronal subpopulation. Brainstem slice recordings were used to detect functional alterations.</p><p><strong>Results: </strong>Several days-long exposure of spinal cord cultures with GlyR aAbs did not change expression levels of proteins building a functional glycinergic synapse. A notable exception was the enhanced expression of presynaptic glycine transporter 2 (GlyT2), possibly reflecting an adaptation to altered synaptic properties. Super-resolution microscopy revealed rather similar binding of patient-derived aAbs to postsynaptic vs presynaptic sites with individual binding preferences. Although characterization of interneurons showed absence of GlyRα1 in some interneuron subpopulations, GlyRα2 and patient serum signals exhibited a significantly higher colocalization in samples with presynaptic preference. This finding identifies GlyRα2 as the hitherto unknown predominant presynaptic GlyR subunit in the spinal cord and a target of patient aAbs. Whole-cell recordings from glycinergic neurons in mouse brainstem slices underscored the functional relevance of presynaptic aAb binding demonstrated by a significant reduction in the frequency of spontaneous and miniature inhibitory postsynaptic potentials.</p><p><strong>Discussion: </strong>In summary, our study is the first to implicate presynaptic defects in the pathophysiology of autoimmune diseases such as SPS and PERM, which are associated with GlyR aAbs. Individually tuned binding preferences for presynaptic and postsynaptic targets thus underlie the rather diverse appearance of clinical symptoms and different therapeutic responses in patients suffering from GlyR autoimmunity.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200364"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11741293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}