Journal of neuroimmunology最新文献

{"title":"Baicalin-Geniposide combination modulates microglia polarization against chronic cerebral ischemia and concomitant kidney injury via the HIF-1α/EPO/NF-κB pathway","authors":"Tian Hu ,&nbsp;Qianqian Sun ,&nbsp;Jiahao Zhang ,&nbsp;Xuewei Zhou ,&nbsp;Jie Gong ,&nbsp;Yuan Li ,&nbsp;Chuan Wang ,&nbsp;Jiping Liu ,&nbsp;Bin Wang","doi":"10.1016/j.jneuroim.2025.578601","DOIUrl":"10.1016/j.jneuroim.2025.578601","url":null,"abstract":"<div><h3>Background</h3><div>Baicalin and geniposide combination (BC/GD), a traditional Chinese medicine pairing, is beneficial for chronic cerebral ischemia (CCI) and kidney injury, but the underlying mechanism remains unknown.</div></div><div><h3>Methods</h3><div>Using network pharmacology, we identified targets and pathways of BC/GD in CCI and kidney injury. Using molecular docking, we discovered the affinity between BC/GD and the key targets HIF-1α, EPOR, and TNF-α. Then, these were verified in SD rats and transwell co-cultures of HMC3 and HK-2 cells.</div></div><div><h3>Results</h3><div>Experimental validation demonstrated that BC/GD ameliorated cerebral and kidney pathological injury, cognitive impairment, and kidney dysfunction, increased cerebral blood flow, inhibited microglia activation and polarization of pro-inflammatory phenotypes, increased the expression of HIF-1α and EPOR, and reduced the phosphorylation of NF-κB and the level of pro-inflammatory factors in CCI rats. Then, in vitro validation experiments, we found that 12.5 μM and 25 μM BC/GD significantly increased the levels of anti-inflammatory factors and modulated the HIF-1α/EPO/NF-κB pathway in oxygen-glucose-deprived HMC3 and HK-2 cells, which was partially antagonized by PX-478, an inhibitor of HIF-1α.</div></div><div><h3>Conclusion</h3><div>BC/GD alleviated cerebral and kidney inflammatory injury, and its mechanism may be related to the modulation of microglia polarization through HIF-1α/EPO/NF-κB.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578601"},"PeriodicalIF":2.9,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143746183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin-1 beta and Interleukin-6 serum concentrations correlate with neuropathy and liver enzyme levels in patients diagnosed with alcohol use disorder","authors":"Michail Papantoniou ,&nbsp;Stylianos Chatzipanagiotou ,&nbsp;Panagiotis Kokotis ,&nbsp;Chrysoula Nikolaou ,&nbsp;Antonios Gargalionis ,&nbsp;Elias Tzavellas ,&nbsp;Thomas Paparrigopoulos ,&nbsp;Michail Rentzos","doi":"10.1016/j.jneuroim.2025.578599","DOIUrl":"10.1016/j.jneuroim.2025.578599","url":null,"abstract":"<div><div>Peripheral neuropathy is a common clinical manifestation in patients diagnosed with alcohol use disorder (AUD). The pathogenesis of alcohol-related neuropathy is under investigation and there are insufficient data to support the hypothesis of a possible immune-mediated pathway. In this study, we correlated serum cytokine concentrations with neurophysiological and biochemical findings and investigated possible risk factors, pathogenetic mechanisms and biomarkers of neuropathy in patients with AUD. Ninety patients with AUD (54 with neuropathy and 36 without neuropathy) and sixty-eight age- and gender-matched healthy subjects (control group) were recruited in this prospective study over a period of three years. Serum concentrations of Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-10, and Tumor Necrosis Factor-alpha (TNF-α), as well as fasting glucose, blood thiamine and liver enzymes levels, were determined upon admission. The mean values of the concentrations of IL-1β, IL-6, IL-8 and TNF-α of patients with AUD were significantly higher than those of the healthy control group. We also found that the mean values of IL-1β and IL-6 concentrations were significantly higher in the group of patients with neuropathy than the patients without polyneuropathy and the healthy control group. Moreover, we found a statistically significant association between higher IL-1β, as well higher IL-6, concentration values and higher liver enzyme levels. Our study suggests that higher concentrations of circulating IL-1β and IL-6 may contribute in the pathophysiology of alcohol-related peripheral neuropathy, and that their concentrations are associated to time- and dose-dependent liver dysfunction.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578599"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738408","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}

{"title":"Potential roles for microglia in drug addiction: Adolescent neurodevelopment and beyond","authors":"Maricela X. Martinez,&nbsp;Stephen V. Mahler","doi":"10.1016/j.jneuroim.2025.578600","DOIUrl":"10.1016/j.jneuroim.2025.578600","url":null,"abstract":"<div><div>Adolescence is a sensitive period for development of addiction-relevant brain circuits, and it is also when people typically start experimenting with drugs. Unfortunately, such substance use may cause lasting impacts on the brain, and might increase vulnerability to later-life addictions. Microglia are the brain's immune cells, but their roles in shaping neural connectivity and synaptic plasticity, especially in developmental sensitive periods like adolescence, may also contribute to addiction-related phenomena. Here, we overview how drugs of abuse impact microglia, and propose that they may play poorly-understood, but important roles in addiction vulnerability and progression.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578600"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143792192","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}

{"title":"Therapeutic potential of Baicalin against experimental obsessive compulsive disorder: Evidence from CSF, blood plasma, and brain analysis","authors":"Abhinay Dhiman ,&nbsp;Divya Choudhary ,&nbsp;Sidharth Mehan ,&nbsp;Pankaj Kumar Maurya ,&nbsp;Arun Kumar Sharma ,&nbsp;Aakash Kumar ,&nbsp;Ritam Mukherjee ,&nbsp;Sumedha Gupta ,&nbsp;Zuber Khan ,&nbsp;Ghanshyam Das Gupta ,&nbsp;Acharan S. Narula","doi":"10.1016/j.jneuroim.2025.578598","DOIUrl":"10.1016/j.jneuroim.2025.578598","url":null,"abstract":"<div><div>Obsessive-Compulsive Disorder (OCD) is a complex neuropsychiatric condition characterized by recurrent obsessions and compulsions, significantly impacting an individual's functionality and quality of life. This study aimed to explore the neuroprotective and therapeutic potential of baicalin, a flavonoid with known antioxidant, anti-inflammatory, and neurotropic properties, in an animal model of OCD induced by 8-OH-DPAT (8HPAT). The research utilized in silico docking studies and in vivo experiments to assess baicalin's interactions with key intracellular targets: SIRT-1, Nrf2, HO-1, and PPAR-gamma, and its effects on neurochemical, neurobehavioral, and histopathological parameters. In silico results indicated a strong binding affinity of baicalin for SIRT-1, Nrf2, HO-1, and PPAR-gamma, suggesting potential regulatory roles in antioxidant and anti-inflammatory pathways. In-vivo findings demonstrated that baicalin, administered at doses of 50 mg/kg and 100 mg/kg, significantly alleviated OCD-like behaviours, including excessive lever pressing, marble burying, and compulsive checking. Baicalin treatment normalized serotonin and dopamine levels and reduced glutamate levels in the brain, restoring neurotransmitter balance. Furthermore, baicalin decreased inflammatory cytokines (TNF-alpha and IL-1 beta), improved complete blood count profile, and gross morphological and histopathological alterations by restoring neuronal density and cellular integrity in affected brain regions. Combining baicalin with fluvoxamine (10 mg/kg) showed synergistic effects, further enhancing neuroprotective outcomes. These results suggest that baicalin holds promise as a potential therapeutic agent for OCD, warranting further clinical investigation to explore its efficacy and underlying mechanisms in human subjects. The findings underscore the importance of targeting intracellular pathways and neurotransmitter systems in developing effective treatments for OCD and related neuropsychiatric disorders.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578598"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738407","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}

{"title":"Comparison of clinical features of aquaporin-4 positive neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein associated disorder (MOGAD), and double seronegative NMOSD - A single center experience","authors":"Melike Cakan ,&nbsp;Ezgi Demirel ,&nbsp;Barışcan Cimen ,&nbsp;Nazire Pınar Acar Özen ,&nbsp;İlksen Çolpak ,&nbsp;Rana Karabudak ,&nbsp;Aslı Tuncer","doi":"10.1016/j.jneuroim.2025.578591","DOIUrl":"10.1016/j.jneuroim.2025.578591","url":null,"abstract":"<div><div>This retrospective study investigates Aquaporin-4 Antibody Positive Neuromyelitis Optica Spectrum Disorder (NMOSD), Myelin Oligodendrocyte Glycoprotein Associated Disorder (MOGAD), and Seronegative NMOSD at a tertiary care university hospital, over a 13 year period (November 2010 to November 2023) involving 78 patients. It distinguishes between the clinical and radiological features of AQP4 + NMOSD (41 patients, 52.5 %), MOGAD (22 patients, 28.2 %), and Seronegative NMOSD (15 patients, 19.3 %). A significant female majority was noted in AQP4+ NMOSD (90.2 %) compared to MOGAD (45.5 %) and Seronegative NMOSD (66.7 %). Age of disease onset and annualized relapse rates were similar across groups. Myelitis was a common initial symptom in AQP4+ NMOSD (48.8 %) and Seronegative NMOSD (40 %), but less so in MOGAD (18.2 %). Optic neuritis was more frequent in MOGAD (68.2 %) and Seronegative NMOSD (53.3 %) than AQP4+ NMOSD (31.7 %). Relapsing disease was less observed in MOGAD (57.1 %) compared to the other groups. Time to the first relapse varied: 12 months for Seronegative NMOSD, 18 months for AQP4+ NMOSD, and 7 months for MOGAD. A higher incidence of autoimmune disorders was found in AQP4+ NMOSD (36.6 %) versus MOGAD (9.5 %). This study delineates a pronounced female and concurrent autoimmune disorder predominance in AQP4+ NMOSD compared to seronegative NMOSD and MOGAD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578591"},"PeriodicalIF":2.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817238","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}

{"title":"Ofatumumab for the treatment of COVID-19-associated autoimmune encephalitis: A case report","authors":"Zhuoran Wang ,&nbsp;Xiaoping Du ,&nbsp;Qiong Wang ,&nbsp;Yating Zhang ,&nbsp;Junhong Guo ,&nbsp;Huifang Wang","doi":"10.1016/j.jneuroim.2025.578590","DOIUrl":"10.1016/j.jneuroim.2025.578590","url":null,"abstract":"<div><div>Autoimmune encephalitis is a rare but severe complication of Coronavirus disease 2019 (COVID-19) infection. Typically, treatment involves immunomodulatory approaches such as steroids, intravenous immunoglobulin (IVIG), or plasma exchange. While for some patients, the above treatment is not effective. Here, we report a case of COVID-19-associated encephalitis, who exhibited cognitive impairment, epileptic seizures, tachycardia, and diaphoresis, with cranial MRI findings resembling those seen in limbic encephalitis. Initially, the patient exhibited a suboptimal response to antiviral therapy, high-dose steroids, and IVIG treatment. Nevertheless, his clinical symptoms and cranial MRI abnormalities markedly improved following the administration of Ofatumumab. Administering Ofatumumab early in COVID-19-related autoimmune encephalitis may benefit patients more.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578590"},"PeriodicalIF":2.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143706296","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}

{"title":"Neuroinflammation and schizophrenia: The role of Toxoplasma gondii infection and astrocytic dysfunction","authors":"Abigail Everett,&nbsp;Hany M. Elsheikha","doi":"10.1016/j.jneuroim.2025.578588","DOIUrl":"10.1016/j.jneuroim.2025.578588","url":null,"abstract":"<div><div>Obligate intracellular pathogens such as the protozoan <em>Toxoplasma gondii</em> exploit host cell mechanisms to facilitate their survival and replication. While <em>T. gondii</em> can infect any nucleated mammalian cell, it exhibits a particular affinity for central nervous system cells, including neurons, astrocytes, and microglia. Among these, astrocytes play a pivotal role in maintaining neuroimmune balance, and their infection by <em>T. gondii</em> induces structural and functional alterations. Emerging evidence suggests that these changes may contribute to the pathophysiology of schizophrenia (SCZ). Although a direct causal link between <em>T. gondii</em>-induced astrocytic dysfunction and SCZ remains unproven, infection has been associated with increased kynurenic acid production, elevated dopamine levels, and heightened inflammatory cytokines—all of which are implicated in SCZ pathology. Additionally, <em>T. gondii</em> infection disrupts crucial neurobiological processes, including <em>N</em>-methyl-<span>d</span>-aspartate receptor signaling, blood-brain barrier integrity, and gray matter volume, further aligning with SCZ-associated neuropathology. This review underscores the need for targeted research into <em>T. gondii</em>-mediated astrocytic dysfunction as a potential factor in SCZ development. Understanding the mechanistic links between <em>T. gondii</em> infection, astrocytic alterations, and psychiatric disorders may open new avenues for therapeutic interventions.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578588"},"PeriodicalIF":2.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of androgen modifying therapies on disease activity in older men with multiple sclerosis","authors":"Burcu Zeydan ,&nbsp;Nur Neyal ,&nbsp;Nabeela Nathoo ,&nbsp;Manu Rangachari ,&nbsp;Elizabeth J. Atkinson ,&nbsp;Jiye Son ,&nbsp;Brittani L. Conway ,&nbsp;W. Oliver Tobin ,&nbsp;B. Mark Keegan ,&nbsp;Brian G. Weinshenker ,&nbsp;Kejal Kantarci ,&nbsp;Jiwon Oh ,&nbsp;Orhun H. Kantarci","doi":"10.1016/j.jneuroim.2025.578589","DOIUrl":"10.1016/j.jneuroim.2025.578589","url":null,"abstract":"<div><h3>Background</h3><div>Anti-inflammatory properties of androgens were assessed in animal models, but only several clinical studies investigated the effects of androgen on multiple sclerosis (MS). Inflammatory activity in MS often attenuates with aging, and androgen modifying therapies (AMT), which mimic decreased androgen levels, are frequently used in older men. We aimed to investigate if the number of disease activity events would increase in older (≥55 years) male persons with MS (MPwMS) who are on AMT.</div></div><div><h3>Methods</h3><div>MPwMS with AMT initiation ≥55 years (AMT; <em>n</em> = 60) and without AMT history (no-AMT; <em>n</em> = 80) were included from a clinical-based observational study cohort. <em>Clinical</em> (relapses), <em>Radiological</em> (new lesions), and <em>Disease</em> (relapses and/or new lesions) <em>activity</em> events were evaluated before and after the age at AMT initiation in AMT and no-AMT groups.</div></div><div><h3>Results</h3><div>Age at MS onset, progressive MS rate and treatment frequencies were similar between the groups. When events before and after the age at AMT initiation (mean = 65.0 ± 7.0 years) were compared, there was a drop in the percentage of individuals with <em>Clinical</em> (38.5 % vs. 10 %), <em>Radiological</em> (46.2 % vs. 40 %) and <em>Disease</em> (62.8 % vs. 40 %) <em>activity</em> events in the no-AMT group. In the AMT group, the percentage of individuals with <em>Clinical activity</em> events was not as dramatically decreased (33.3 % vs. 22.2 %), <em>Radiological activity</em> events was increased (35.2 % vs. 46.7 %), and <em>Disease activity</em> events was sustained (51.9 % vs. 51.1 %). The probability of <em>Disease activity</em> was higher in the AMT group at 3 years of AMT initiation (40 % vs. 29 %) compared to the no-AMT group matched for disease duration, but the difference was not significant (<em>p</em> = 0.582).</div></div><div><h3>Conclusions</h3><div>Rather than the expected decrease in disease activity with age, MPwMS receiving AMT experienced sustained or increased disease activity, particularly at &gt;65 years. Close clinical monitoring of MPwMS starting on these medications is necessary.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578589"},"PeriodicalIF":2.9,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679417","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}

{"title":"Peripheral and central inflammation in depression: How large is the gap and can we bridge it with PET neuroimaging and neural-derived extracellular vesicles?","authors":"Cristian-Daniel Llach ,&nbsp;Gia Han Le ,&nbsp;Hiya Shah ,&nbsp;Liz M. Marcato ,&nbsp;Elisa Brietzke ,&nbsp;Hartej Gill ,&nbsp;Aniqa Tabassum ,&nbsp;Sebastian Badulescu ,&nbsp;Joshua D. Rosenblat ,&nbsp;Roger S. McIntyre ,&nbsp;Rodrigo B. Mansur","doi":"10.1016/j.jneuroim.2025.578587","DOIUrl":"10.1016/j.jneuroim.2025.578587","url":null,"abstract":"<div><div>Major depressive disorder (MDD) presents as a multifaceted syndrome with complex pathophysiology and variable treatment responses, posing significant challenges in clinical management. Neuroinflammation is known to play pivotal mechanism in depression, linking immune responses with central nervous system (CNS) dysfunction. This review explores the interplay between peripheral and central inflammatory processes in MDD, emphasizing discrepancies in biomarker validity and specificity. While peripheral markers like cytokines have historically been investigated as proxies for neuroinflammation, their reliability remains contentious due to inconsistent findings, lack of correlation with neuroinflammatory markers, the influence of confounding variables, and the role of regulatory mechanism within the CNS. Additionally, the human brain shows a pattern of regionalized inflammation. Current methodologies for investigating neuroinflammation in humans in vivo, including neural-derived extracellular vesicles (EVs) and positron emission tomography (PET) neuroimaging using translocator protein, offer promising avenues while facing substantial limitations. We propose that future research in MDD may benefit from combined microglia-derived EV-TSPO PET neuroimaging analyses to leverage the strengths and mitigate the limitations of both individual methods.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578587"},"PeriodicalIF":2.9,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143737788","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}

{"title":"Satralizumab treatment in patients with AQP4-IgG–seropositive neuromyelitis optica spectrum disorder after rituximab treatment: A case series","authors":"Hesham Abboud ,&nbsp;Brian Steingo ,&nbsp;Diana Vargas ,&nbsp;Julie Patel ,&nbsp;Nancy Nealon ,&nbsp;Mary Alissa Willis ,&nbsp;Yang Mao-Draayer ,&nbsp;Dmitry Khaitov ,&nbsp;Michelle Tsai ,&nbsp;Angie Kim ,&nbsp;Krupa Pandey ,&nbsp;Michael Levy ,&nbsp;Negar Molazadeh ,&nbsp;Rebecca S. Romero ,&nbsp;Lisa Ferayorni ,&nbsp;Shervin Gholizadeh","doi":"10.1016/j.jneuroim.2025.578585","DOIUrl":"10.1016/j.jneuroim.2025.578585","url":null,"abstract":"<div><h3>Background</h3><div>The US Food and Drug Administration approved satralizumab for use in adult patients with aquaporin-4 immunoglobulin G–positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) in 2020, but real-world data are limited. The objective of this case series is to describe the experience with satralizumab in adult patients with AQP4-IgG+ NMOSD who previously received rituximab.</div></div><div><h3>Methods</h3><div>Case information for patients with AQP4-IgG+ NMOSD who had received satralizumab for ≥6 months was obtained from US healthcare providers from April 1, 2022, to September 30, 2023. Patient characteristics, examination findings, diagnostic tests, treatment response and adverse events were recorded. Patients who received satralizumab after discontinuing treatment with rituximab were included in this case series.</div></div><div><h3>Results</h3><div>Twenty patients were included, and their ages ranged from 19 to 70 years. Overall, 45 % of patients self-identified as Black/African American, 40 % as White, 10 % as Asian and 5 % as multiracial. Time since confirmed NMOSD diagnosis ranged from 4 to 17 years. Median (range) duration of rituximab treatment was 50 (12–162) months. The main reasons for switching to satralizumab were intolerance (60 %) to and inadequate disease control (25 %) with rituximab. The majority of patients (70 %) received satralizumab for ≥24 months and as monotherapy (90 %). All 20 patients were free from radiographically confirmed relapses with satralizumab. Overall, patients maintained disease control with satralizumab, and adverse events primarily included asymptomatic laboratory abnormalities. Two patients permanently discontinued satralizumab due to adverse events.</div></div><div><h3>Conclusions</h3><div>In this retrospective case series, satralizumab was effective and well tolerated in patients with NMOSD who switched due to ineffectiveness and/or poor tolerability of rituximab. These outcomes align with the long-term efficacy and safety outcomes with satralizumab in the Phase III SAkura clinical trials.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578585"},"PeriodicalIF":2.9,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}