Journal of neuroimmunology最新文献

{"title":"Sex differences in the neuroimmune response following heavy, binge-like alcohol exposure in adolescent rats","authors":"Catherine E. Van Doorn ,&nbsp;Natalie Nawarawong ,&nbsp;Deann M. Hopkins ,&nbsp;Hui Peng ,&nbsp;James R. Pauly ,&nbsp;Kimberly Nixon","doi":"10.1016/j.jneuroim.2025.578742","DOIUrl":"10.1016/j.jneuroim.2025.578742","url":null,"abstract":"<div><div>Adolescents who consume alcohol show a high prevalence of binge drinking, which has been linked to brain damage and neuroimmune reactions that increase risk for developing an alcohol use disorder (AUD). Adolescent female drinking patterns have surpassed males, yet little is known about damaging effects of alcohol in females. Known sex differences in neuroimmune reactivity, specifically microglial reactivity, suggest that the female brain will differ from males. Therefore, we examined indicators of neuroimmune activation and neurodegeneration following 2 days of heavy, bingelike exposure in adolescent male and female rats. Translocator protein 18kD (TSPO) expression assessed by [³H]PK-11195 autoradiography revealed that adolescent female rats showed a brief and immediate response in the thalamus, while male rats showed a delayed and sustained increase in the thalamus and hippocampus versus same-sex controls. Neurodegeneration assessed by Fluoro-Jade-B (FJB) dye showed that alcohol-induced cell death was modest for both sexes. Males showed cell death in the entorhinal cortex while females showed greater cell death in the perirhinal and piriform cortices. Additional neuroimmune measures of pro-inflammatory cytokine, IL-6, was decreased in the hippocampus and entorhinal cortex a week after alcohol exposure in females only. No changes in brain-derived neurotrophic factor (BDNF) were found in either sex or region. Overall, these experiments show adolescent females and males display unique neuroimmune responses and neurodegeneration profiles following heavy binge-like exposure. These data imply that females show a impaired neuroimmune response to alcohol that could contribute to sex differences in damage and deficits caused by alcohol.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"409 ","pages":"Article 578742"},"PeriodicalIF":2.5,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005085","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":"Treatment strategy for myasthenia gravis with GAD65-IgG associated neurological disorders: A case report","authors":"Xiao-Na Xu ,&nbsp;Wen-Jun Luo ,&nbsp;Hui-Ning Li ,&nbsp;Xin Li ,&nbsp;Jun-Ping Wang ,&nbsp;Wei Jiang ,&nbsp;Shu Yang ,&nbsp;Chun-Sheng Yang","doi":"10.1016/j.jneuroim.2025.578741","DOIUrl":"10.1016/j.jneuroim.2025.578741","url":null,"abstract":"<div><div>We present a clinically instructive case of a 50-year-old woman with acetylcholine receptor (AChR) antibody-positive generalized myasthenia gravis (MG) who subsequently developed glutamic acid decarboxylase 65 (GAD65) antibody-associated neurological disorders alongside a type B2 thymoma. This rare coexistence highlights the profound immune dysregulation induced by thymomas, wherein loss of self-tolerance emergence multiple concurrent autoimmune phenomena. The patient's favorable response to multimodal immunotherapy—including efgartigimod, high-dose corticosteroids, and rituximab—underscores the therapeutic imperative for early, targeted immunomodulation in such complex neuroimmunological syndromes. As no standardized treatment currently exists for MG with GAD65-IgG-associated neurological disorders, this case provides critical clinical insights into both the diagnostic and therapeutic approach for this complex disease.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"409 ","pages":"Article 578741"},"PeriodicalIF":2.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005084","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":"Serum neurofilament light chain as a prognostic biomarker of glial fibrillary acidic protein autoimmunity","authors":"Akio Kimura ,&nbsp;Akira Takekoshi ,&nbsp;Yoichi Maekawa ,&nbsp;Keiko Tanaka ,&nbsp;Yoshihisa Yamano ,&nbsp;Kuniaki Saito ,&nbsp;Yasuko Yamamoto ,&nbsp;Masao Takemura ,&nbsp;Takayoshi Shimohata","doi":"10.1016/j.jneuroim.2025.578739","DOIUrl":"10.1016/j.jneuroim.2025.578739","url":null,"abstract":"<div><div>This study investigated whether serum neurofilament light chain (NFL) levels could predict the prognosis of patients with Glial Fibrillary Acidic Protein Autoimmunity (GFAP-A). The study included 54 patients diagnosed with GFAP-A at Gifu University Graduate School of Medicine between June 2019 and October 2023. Patients with other neurological diseases or antineuronal antibodies were excluded. NFL levels in serum and cerebrospinal fluid (CSF) samples at admission were measured, and their association with patient prognosis was analyzed. Patients with an unfavorable outcome were defined as those with a modified Rankin Scale (mRS) score of 3 or higher at 6 months after admission. Results showed that 13 patients (24 %) had an unfavorable outcome. Serum NFL levels at admission were higher in patients with an unfavorable outcome [median (range): 191 (39–409) pg/mL] compared to those with a favorable outcome (mRS score ≤ 2) [64 (14–341) pg/mL] (<em>P</em> &lt; 0.001). Similarly, CSF NFL levels were higher in patients with a poor prognosis [21,932 (9673–34,324) pg/mL] compared to those with a favorable outcome [8014 (986–55,130) pg/mL] (P &lt; 0.001). Binary logistic regression analysis, adjusted for age, duration from onset to admission, and mRS score at admission, identified serum NFL level as an independent predictor of unfavorable outcome at the 6-month time point (OR, 1.0114; 95 % CI [1.0014–1.0214]; <em>P</em> = 0.0250). ROC analysis indicated that serum NFL level at admission is a sensitive predictor of unfavorable outcome for GFAP-A (AUC, 0.853; sensitivity, 92.3 %; specificity, 73.2 %). In conclusion, serum NFL levels at diagnosis may serve as an important prognostic biomarker for GFAP-A.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578739"},"PeriodicalIF":2.5,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922589","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":"Next-generation approaches in autoimmune encephalitis diagnosis: A multi-omics perspective","authors":"Mingjing Zhao ,&nbsp;Jing Li ,&nbsp;LiWen Jin ,&nbsp;Zhaohui Luo","doi":"10.1016/j.jneuroim.2025.578740","DOIUrl":"10.1016/j.jneuroim.2025.578740","url":null,"abstract":"<div><div>Autoimmune encephalitis (AE) is a group of autoantibody-mediated inflammatory disorders of the central nervous system (CNS) that often present with cognitive deficits, behavioral abnormalities, and seizures. The subtypical variability of AE calls for individualized treatments based on specific antibodies and clinical manifestations. Early and accurate diagnosis and standardized treatment are essential to improve prognosis and promote neurological recovery. Currently, clinical diagnosis of AE relies on the detection of specific antibodies in serum and cerebrospinal fluid (CSF). However, there is usually a delay in this approach, leading to late initiation of treatment, which may result in patients' disease progression yet still not effectively treated. For example, for some specific subtypes of AE, existing antibody tests may not capture all potential markers in time, making early diagnosis and subtyping challenging. In addition, certain AE patients have low antibody levels that make it difficult to confirm the diagnosis with conventional assays, resulting in a delayed diagnosis. Therefore, there is an urgent need for new methods to improve the efficiency of differential diagnosis based on the sensitivity, specificity, or accessibility issues faced by antibody-based diagnosis.</div><div>With the help of multi-omics technologies, potential biomarkers of AE can be identified through genomic, proteomic, and metabolomic analyses, leading to improved diagnosis. Multi-omics technologies have demonstrated great potential in the diagnosis and treatment of AE, especially in revealing new markers and improving early diagnosis, but the limitations of technological complexity high cost, and the problem of clinical applicability still need to be overcome. In the future, with technological advances and cost reductions, multi-omics approaches are expected to become an important tool for the early diagnosis of AE and promote more accurate and timely treatment.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578740"},"PeriodicalIF":2.5,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922590","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":"Characterizing the relationship between FLAIR hyper-rim lesions and paramagnetic rim lesions in multiple sclerosis","authors":"Yang Tang ,&nbsp;Huajiao Wang ,&nbsp;Xiaohua Wang ,&nbsp;Zichun Yan ,&nbsp;Qiyuan Zhu ,&nbsp;Ting Yin ,&nbsp;Yuhui Xu ,&nbsp;Yiqiu Wei ,&nbsp;Bin Yang ,&nbsp;Zhuowei Shi ,&nbsp;Yongmei Li","doi":"10.1016/j.jneuroim.2025.578738","DOIUrl":"10.1016/j.jneuroim.2025.578738","url":null,"abstract":"<div><div>Paramagnetic rim lesions (PRLs), identified using susceptibility-sensitive sequences, are established prognostic imaging markers for multiple sclerosis (MS). However, susceptibility-sensitive sequences are not yet routinely performed in many clinical centers. We aim to investigate an imaging feature observed on conventional T2 fluid-attenuated inversion recovery (FLAIR) sequences, termed “FLAIR hyper-rim”, and explore its association with PRLs. This study included 61 relapsing-remitting MS (RRMS) and 35 healthy controls. Based on the presence or absence of paramagnetic rim in susceptibility-sensitive images (PRL+/−) and FLAIR hyper-rim sign in T2-FLAIR images (Rim+/−), white matter (WM) lesions were classified into four subgroups: (1) PRL + Rim+; (2) PRL + Rim-; (3) PRL-Rim+; (4) PRL-Rim-. Differences in lesion volume and microstructural damage were compared, based on diffusion kurtosis imaging (DKI) parameters, including kurtosis fractional anisotropy (KFA), mean kurtosis (MK), axial kurtosis (AK), and radial kurtosis (RK). The correlations between lesion load and clinical scale scores and brain volume were further investigated. 1109 WM lesions were analyzed, including 338 PRLs and 300 FLAIR hyper-rim lesions. Of 300 FLAIR hyper-rim lesions, 197 (65.7 %) co-localized with a PRL, and 197/338 (58.3 %) PRLs co-localized with a FLAIR hyper-rim lesion. Considering the chance-level overlap, we further calculated the Jaccard index (44.7 %, 95 % CI: 39.8–49.5), and Cohen's kappa (κ = 0.463, 95 % CI: 0.408–0.518), both indicating a moderate association. The PRL + Rim+ group exhibited the lowest AK and RK values, significantly different from those of other three groups (all <em>P</em> &lt; 0.05). Additionally, the PRL-Rim+ group exhibited lower MK, AK and RK values compared to the PRL-Rim- group (all <em>P</em> &lt; 0.05). Furthermore, FLAIR hyper-rim lesions were negatively related to cognitive test and brain volume. FLAIR hyper-rim lesions appear to represent a subtype of MS lesions characterized by more severe tissue damage and may help identify lesions more likely to be PRLs, although their predictive value requires further validation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578738"},"PeriodicalIF":2.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144919848","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":"The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise","authors":"Maria Carolina Machado da Silva ,&nbsp;Antônio Carlos Pinheiro de Oliveira ,&nbsp;Eduardo Candelario-Jalil ,&nbsp;Habibeh Khoshbouei","doi":"10.1016/j.jneuroim.2025.578736","DOIUrl":"10.1016/j.jneuroim.2025.578736","url":null,"abstract":"<div><div>Methamphetamine use disorder remains a significant public health concern, impacting neuronal function, immune responses, and vascular integrity. Of particular interest is methamphetamine's disruption of the blood–brain barrier (BBB), a key event that triggers neuroimmune dysfunction and the development of neurodegenerative conditions. While the systemic effects of methamphetamine are well-characterized, the mechanism(s) governing its dysregulation of BBB physiology remain poorly understood. Emerging evidence suggests that the methamphetamine-induced production of tumor necrosis factor (TNF), occurring both in the periphery and within the central nervous system, triggers a cascade of molecular events that compromises BBB permeability. This review provides a comprehensive overview of current findings on the cross interaction between methamphetamine and the BBB, with particular emphasis on the potential role of TNF in dysregulation of BBB permeability and dysfunction. By elucidating the complex interplay between methamphetamine, TNF, and the BBB, we aim to inform the development of targeted interventions and preventative strategies to mitigate methamphetamine-induced neurovascular and neuroimmune dysfunction.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"409 ","pages":"Article 578736"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989409","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 prednisolone monotherapy vs. tacrolimus combination in NMOSD: Efficacy, safety, and optimal therapeutic timing","authors":"Keito Ishihara ,&nbsp;Hiroyuki Naito ,&nbsp;Takamichi Sugimoto ,&nbsp;Masahiro Nakamori ,&nbsp;Yu Yamazaki ,&nbsp;Kazuhide Ochi ,&nbsp;Hirofumi Maruyama","doi":"10.1016/j.jneuroim.2025.578737","DOIUrl":"10.1016/j.jneuroim.2025.578737","url":null,"abstract":"<div><div>Tacrolimus (TAC) has been considered an effective treatment for neuromyelitis optica spectrum disorder (NMOSD), a neuroinflammatory disease associated with aquaporin-4 antibodies. This retrospective cohort study aimed to assess the efficacy and safety of TAC-based therapies compared with prednisolone (PSL) monotherapy in preventing relapse and optimizing treatment timing. Forty-one patients with NMOSD treated at Hiroshima University Hospital between 2015 and 2022 were included in the analysis. These patients met the 2015 International Consensus Diagnostic Criteria and received either TAC or PSL for at least 6 months. Patients treated with TAC, either alone or in combination with PSL, demonstrated significantly lower relapse rates (<em>p =</em> 0.002) and annualized relapse rates (<em>p =</em> 0.027) than those treated with PSL monotherapy. Furthermore, TAC recipients required lower PSL doses (<em>p =</em> 0.029), and two patients successfully discontinued PSL entirely. Importantly, initiating TAC within 3 months of starting PSL further reduced relapse rates compared with later initiation (<em>p =</em> 0.040). Although two TAC-treated patients experienced relapses leading to therapy discontinuation, no adverse events led to therapy cessation. These findings suggest that TAC may suppress relapse rates and enable reduction of PSL dosage, without apparent safety concerns. Early TAC initiation may also be associated with lower relapse rates.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578737"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144916460","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":"Serum from patients with MuSK antibody-positive myasthenia gravis triggers transcriptomic changes leading to muscle atrophy and weakness in human myotube cells","authors":"Keisuke Tanaka ,&nbsp;Akiyuki Uzawa ,&nbsp;Manato Yasuda ,&nbsp;Yosuke Onishi ,&nbsp;Hiroyuki Akamine ,&nbsp;Hideo Handa ,&nbsp;Etsuko Ogaya ,&nbsp;Shota Miyake ,&nbsp;Masayuki Baba ,&nbsp;Hiroto Abe ,&nbsp;Koki Nagaoka ,&nbsp;Yuko Nakatake-Furuie ,&nbsp;Yoshichika Katsura ,&nbsp;Kenichi Serizawa ,&nbsp;Satoshi Kuwabara","doi":"10.1016/j.jneuroim.2025.578735","DOIUrl":"10.1016/j.jneuroim.2025.578735","url":null,"abstract":"<div><div>Myasthenia gravis (MG) is an autoimmune disease characterized by autoantibodies targeting the acetylcholine receptor (AChR) or muscle-specific tyrosine kinase (MuSK). These autoantibodies inhibit ACh signal transmission at the neuromuscular junction, leading to muscle weakness and fatigue. Anti–MuSK antibody-positive MG (MuSK+MG) appears more rarely than anti–AChR antibody-positive MG but more frequently results in muscle atrophy. However, the underlying mechanism is unknown. In this study, we analyzed whether serum from MuSK+MG patients has any pathogenic effect on cultured myotube cells. Primary human skeletal muscle myoblasts were differentiated into myotubes, which were then treated with serum from healthy control individuals or MuSK+MG patients. After one day, RNA-seq analysis and Western blotting were performed and myotube diameters were measured. Calcium dynamics following caffeine stimulation was also assessed. Comparing myotube cells treated with healthy control serum with those treated with serum from MuSK+MG patients, RNA-seq analysis showed suppression of pathways associated with muscle function and Western blotting analysis revealed reduced expression of Type II myosin heavy chain. These changes are consistent with muscle atrophy and weakness, although myotube diameter remained unchanged. Caffeine stimulation induced higher cytoplasmic calcium levels. Expression of sarcomere components was significantly reduced. Serum from MuSK+MG patients directly affected gene and protein expression in cultured human myotube cells, leading to changes associated with muscle atrophy and weakness. These findings suggest that there are mechanisms in addition to impaired ACh signal transmission at the neuromuscular junction that can cause muscle weakness and fatigue in MG patients.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578735"},"PeriodicalIF":2.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908237","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":"Neuropathic pain in CASPR2 antibody disease spectrum: A systematic review","authors":"Sara Cornacchini ,&nbsp;Massimiliano Ugo Verza ,&nbsp;Mattia Schiavolin ,&nbsp;Gregorio Spagni ,&nbsp;Ebe Schiavo ,&nbsp;Antonio Lotti ,&nbsp;Antonio Farina ,&nbsp;Deborah Leccese ,&nbsp;Alessandro Barilaro ,&nbsp;Luca Massacesi ,&nbsp;Valentina Damato","doi":"10.1016/j.jneuroim.2025.578734","DOIUrl":"10.1016/j.jneuroim.2025.578734","url":null,"abstract":"<div><h3>Background</h3><div>Contactin-associated protein-like 2 (CASPR2) antibodies are mainly linked to acquired neuromyotonia, limbic encephalitis and Morvan syndrome. Nevertheless, neuropathic pain is increasingly reported, though data on its characteristics remain limited. Here, we describe a patient with isolated neuropathic pain associated with CASPR2 antibodies and we conducted a systematic review to better define this relevant presentation.</div></div><div><h3>Methods</h3><div>Index case was reported following CARE guidelines. The systematic review was performed on MEDLINE, Embase, and Cochrane, according to the updated PRISMA statement guidelines.</div></div><div><h3>Results</h3><div>The literature review identified 216 patients with neuropathic pain in the context CASPR2 antibody disease spectrum, with isolated pain described in only 16/216 (7.4 %) cases. Pain was typically severe and presented as distal burning pain (74/147, 50.3 %), widespread pain with myalgia and cramps (31/147, 21.1 %), or severe back pain radiating to the legs (13/147, 8.8 %). Peripheral nerve hyperexcitability was found in 50/76 (65.8 %) of patients, while small nociceptive fiber dysfunction was identified in 16/19 (84.2 %). Immunotherapy, especially second line treatments, improved pain in 85.4 % (76/89) of cases, with complete remission of symptoms in 34/89 (38.2 %), while <del>s</del>ymptomatic treatment helped 55.1 % (27/49) of patients, with complete response in 10/49 (20.4 %). Long-term therapy was often needed, and relapses occurred in 5.2 % (5/96) after discontinuation.</div></div><div><h3>Conclusions</h3><div>Neuropathic pain appears to be a suggestive and relevant symptom in CASPR2 disease. Although rare, it can be the solely clinical feature of the disease. Testing for CASPR2 antibodies should be included in the screening of patients with neuropathic pain as in these cases rapid initiation of immunotherapy and escalation to second-line treatments can be highly effective.</div></div><div><h3>Registration information</h3><div>The systematic review protocol was registered in the PROSPERO website [Protocol number CRD42024582950].</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578734"},"PeriodicalIF":2.5,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913296","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":"Apathy in autoimmune GFAP Astrocytopathy: A case series and literature review","authors":"Yuji Tomizawa ,&nbsp;Hanna Okada ,&nbsp;Mayu Miyachi ,&nbsp;Yasunobu Hoshino ,&nbsp;Davide Cossu ,&nbsp;Akio Kimura ,&nbsp;Takayoshi Shimohata ,&nbsp;Nobutaka Hattori","doi":"10.1016/j.jneuroim.2025.578733","DOIUrl":"10.1016/j.jneuroim.2025.578733","url":null,"abstract":"<div><h3>Background</h3><div>Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is a newly recognized disease characterized by the presence of GFAPα antibodies in cerebrospinal fluid and linear perivascular radial enhancement on contrast-enhanced MRI. Apathy, although infrequently reported, has emerged as a potential core symptom of GFAP astrocytopathy, distinct from cognitive dysfunction, depression, and consciousness disturbances.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the prevalence and characteristics of apathy in GFAP astrocytopathy cases treated at our institution.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed six cases of GFAP astrocytopathy diagnosed at our hospital, focusing on the presence and course of apathy. Apathy was assessed based on Marin and Stuss's criteria, which define it as a marked decrease in spontaneity not attributable to general physical condition, consciousness disturbance, cognitive impairment, or mood disorder. Imaging studies, including MRI and brain perfusion SPECT, were conducted to explore the potential anatomical correlates of apathy.</div></div><div><h3>Results</h3><div>Of the six cases, four presented with apathy. All cases showed improvement following treatment. MRI and SPECT analyses revealed decreased blood flow in regions associated with apathy, such as the anterior cingulate cortex, orbitofrontal cortex, thalamus, and basal ganglia.</div></div><div><h3>Conclusion</h3><div>Apathy appears to be a relatively common and potentially core symptom in GFAP astrocytopathy, often associated with specific brain regions implicated in its pathophysiology. Recognizing and addressing apathy in these patients could facilitate earlier diagnosis and more targeted therapeutic strategies. Further research with larger cohorts and standardized diagnostic criteria is needed to deepen our understanding of apathy in GFAP astrocytopathy.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578733"},"PeriodicalIF":2.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893280","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}