Journal of neuroimmunology最新文献

{"title":"Exploring the effectiveness of cytarabine in people living with HIV with progressive multifocal leukoencephalopathy: a retrospective cohort study in Chongqing, China","authors":"Min Liu ,&nbsp;Huan Li ,&nbsp;Mei Li,&nbsp;Qin Zeng,&nbsp;Hong-Hong Yang","doi":"10.1016/j.jneuroim.2025.578676","DOIUrl":"10.1016/j.jneuroim.2025.578676","url":null,"abstract":"<div><h3>Background</h3><div>The incidence of progressive multifocal leukoencephalopathy (PML) in people living with HIV (PLWH) is approximately 2 %–4 % globally, and there is currently no effective therapeutic strategy. Cytarabine has been reported to increase the survival probability of PLWH with PML; however, its effectiveness remains controversial. The present study aimed to explore whether cytarabine improves the outcomes of PLWH with PML.</div></div><div><h3>Methods</h3><div>We retrospectively collected data from PLWH who were admitted to the hospital and were diagnosed with PML from January 1, 2019, to October 31, 2023, in Chongqing, China, and then stratified the patients into two groups according to whether they did or did not receive cytarabine treatment. The clinical outcomes and mortality rates were assessed.</div></div><div><h3>Results</h3><div>A total of 41 patients were included in our study. The median age at the time of hospital admission was 44 years [interquartile range (IQR), 36–51]. The patient cohort had a median CD4+ T-cell count of 68.0 (38.5–109.5) cells/mL and a median HIV viral load of 5.05 (2.53, 5.76) log10 copies/ml. 15 patients received intravenous cytarabine and antiretroviral therapy (ART), and 26 patients did not receive cytarabine (24 patients received ART, and 2 patients did not receive ART). In the cytarabine group, 7 patients (46.7 %) died, 4 patients (26.7 %) improved, 2 patients (13.3 %) stabilized, and 2 patients (13.3 %) worsened. In the noncytarabine group, 15 (57.7 %) patients died, 7 patients (26.9 %) improved, 3 patients (11.5 %) stabilized, and 1 patient (3.9 %) worsened; the clinical outcomes did not significantly differ between the two groups (<em>P</em> &gt; 0.05). The overall mortality rate and 30-day, 90-day, 180-day and one-year mortality rates were lower in the cytarabine group than in the noncytarabine group, but the differences were not significant (<em>P</em> &gt; 0.05).</div></div><div><h3>Conclusions</h3><div>Our results suggest that treatment with cytarabine seems to fail to improve the survival rates of PLWH with PML. Our study is small and cannot definitively rule out cytarabine activity against PML. Future studies in a larger cohort and longer observations are needed.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578676"},"PeriodicalIF":2.9,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144518111","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":"Evolution and significance of neuronal surface autoantibodies after Japanese encephalitis","authors":"Anjan Nibber ,&nbsp;Bridget Wills ,&nbsp;Philippa Pettingill ,&nbsp;Hannah Fox ,&nbsp;Tran Thi Nhu Thuy ,&nbsp;Nguyen Van Vinh Chau ,&nbsp;Patrick Waters ,&nbsp;Rachel Kneen ,&nbsp;Yael Hacohen ,&nbsp;Christopher E. Uy ,&nbsp;Sayaphet Rattanavong ,&nbsp;Mayfong Mayxay ,&nbsp;Audrey Dubot-Pérès ,&nbsp;Manivanh Vongsouvath ,&nbsp;Viengmon Davong ,&nbsp;Vilada Chansamouth ,&nbsp;Koukeo Phommasone ,&nbsp;Bethan Lang ,&nbsp;Paul N. Newton ,&nbsp;Tom Solomon ,&nbsp;Sarosh R. Irani","doi":"10.1016/j.jneuroim.2025.578671","DOIUrl":"10.1016/j.jneuroim.2025.578671","url":null,"abstract":"<div><div>NMDAR-antibody encephalitis can arise as a post-infectious ‘relapse’ following HSV encephalitis. We asked whether a similar condition might occur after Japanese Encephalitis (JE). Cell-based assays for antigen-specific antibodies and IgG binding to the surface of live hippocampal neurons were performed on 13 CSFs and 65 sera, many sampled longitudinally, from 34 Vietnamese children with JE. Three month outcomes were scored according to a pediatric post-encephalitis scale; clinical features focussed on new onset symptoms during the follow-up, blinded to antibody results. Ten/34 children (29 %) had serum antibodies against known neuronal-surface antigens, 4 NMDAR, 4 CASPR2, 1 GABAAR and 1 LGI1, detected from day 23 after onset. In addition, 8/10 (80 %) of these children and 13/24 (54 %) others had antibodies that bound in a distinctive pattern to live hippocampal neurons (HN-Abs), four detected on days 9–12. A relapse was only considered possible in 5 patients, two with specific neuronal surface antibodies (NSAbs). Neither specific NSAbs (<em>p</em> = 1.00) nor HN-Abs (p = 1.00).were more common in patients with possible relapse than in those with unlikely relapse. There was a modest trend towards worse outcome scores in patients with known NSAbs than in the remaining patients (<em>p</em> = 0.089). Antibodies to neuronal surface proteins, known and unknown, are common in children after JE. Caution is urged in defining post-infectious autoimmune encephalitis on the basis of a positive neuronal antibody and new onset symptoms or deterioration following recovery from JE, or in initiating immunotherapy without confirmatory evidence of a time-dependent encephalitic illness defined by published guidelines.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578671"},"PeriodicalIF":2.9,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144524337","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":"Gene prediction link between metabolite-mediated inflammatory factors and vertigo","authors":"Moyan Wang ,&nbsp;Qi Han ,&nbsp;Xin Teng ,&nbsp;Ke Xiang ,&nbsp;Li Sun","doi":"10.1016/j.jneuroim.2025.578675","DOIUrl":"10.1016/j.jneuroim.2025.578675","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the causal relationship between inflammatory factors and vertigo diseases, and to determine and quantify the role of 1400 metabolites as potential mediators.</div></div><div><h3>Methods</h3><div>Using the summary data of the whole genome association study(genome-wide association study, GWAS), two-sample Mendel randomization(Mendelian randomization, MR)analysis was performed on four vertigo diseases and 1400 inflammatory factors predicted by genes.Furthermore, we used two-step MR to quantify the effects of 1400 metabolite-mediated inflammatory factors on vertigo.</div></div><div><h3>Results</h3><div>MR analysis identified higher genes predicted inflammatory factors to increase the risk of vertigo. Reverse studies of inflammatory factors on vertigo have shown that gene-predicted vertigo has no effect on most of the selected inflammatory factors. Metabolites-mediated gene predictions are more associated with inflammatory factors, and mediating effects lack strong evidence support.</div></div><div><h3>Conclusion</h3><div>In summary, our study identified a causal relationship between inflammatory factors and vertigo, where the proportion of effects mediated by blood metabolites and other metabolites is small, but the majority of the effects of inflammatory factors on vertigo remain unclear. Additional risk factors as potential mediating factors require further research. In clinical practice, blood test indicators for patients with vertigo deserve in-depth exploration.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578675"},"PeriodicalIF":2.9,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501919","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":"Occult cartilaginous choristoma in a child with myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis","authors":"Sayaka Enomoto ,&nbsp;Hiroki Tsuchiya ,&nbsp;Yoshiyuki Ayada ,&nbsp;Yoshiki Takai ,&nbsp;Toshiki Takenouchi","doi":"10.1016/j.jneuroim.2025.578674","DOIUrl":"10.1016/j.jneuroim.2025.578674","url":null,"abstract":"<div><div>Myelin oligodendrocyte glycoprotein antibody-associated disease is a central inflammatory demyelinating disorder that cause diverse neurological symptoms. Paraneoplastic neurologic syndromes occur in association with malignant neoplasms and manifest with a wide range of neuropsychiatric symptoms. Paraneoplastic neurological syndrome is rare in myelin oligodendrocyte glycoprotein antibody-associated disease and, when reported, is typically seen in adults. Herein, we report a 3-year-old girl who presented with lower limb paralysis, urinary retention, and seropositivity for myelin oligodendrocyte glycoprotein antibody. Her symptoms did not respond to various immunotherapies. She was incidentally found to have a cartilaginous choristoma in the neck, after surgical resection of which, she showed symptomatic recovery without recurrence. Immunohistochemical analysis of the resected tumor revealed expression of myelin oligodendrocyte glycoprotein within the cartilage tissue. Based on this case experience, children presenting with myelin oligodendrocyte glycoprotein antibody-associated disease who fail to respond to immunotherapies may need prompt screening for occult tumors.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578674"},"PeriodicalIF":2.9,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365253","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 S-nitrosoglutathione reductase inhibitor in B cell-driven experimental autoimmune encephalomyelitis","authors":"Jeseong Won ,&nbsp;Judong Kim ,&nbsp;Fei Qiao ,&nbsp;Avtar K. Singh ,&nbsp;Inderjit Singh","doi":"10.1016/j.jneuroim.2025.578673","DOIUrl":"10.1016/j.jneuroim.2025.578673","url":null,"abstract":"<div><div>We previously reported that S-nitrosoglutathione (GSNO) and GSNO reductase inhibitors, which increase endogenous GSNO, mitigate T cell-dependent experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, by suppressing Th1 and Th17 effector T cells while promoting regulatory T cells (Tregs). In this study, we demonstrate that the GSNO reductase inhibitor (N6022) also alleviates B cell-dependent EAE in C57BL/6 mice immunized with recombinant human myelin oligodendrocyte glycoprotein (rhMOG₁_–₁₂₅). Daily N6022 treatment following disease onset significantly reduced clinical EAE disease symptoms. N6022 treatment increased the number of CD1d^hiCD5⁺ regulatory B cells (Bregs) in the spleen and inhibited B cell expression of the effector cytokine IL-6 while enhancing their expression of the regulatory cytokine IL-10. Accordingly, N6022 reduced the number of pathogenic effector CD4⁺ T cells (Th1 and Th17) in the spleen and decreased the expressions of proinflammatory cytokines associated with these T cells (IFN-γ and IL-17a), and increased the number of Treg cells with increased serum levels of IL-10. N6022 treatment also suppressed B cell maturation into plasma cells, lowering serum autoantibody levels against human MOG₁_–₁₂₅ IgG. Similar observations were made in the spinal cord, where N6022 treatment modulated B cell expression of regulatory versus effector cytokines (IL-10 &gt; IL-6) and the expansion of regulatory versus effector T cells (Treg &gt; Th1/Th17). These findings document that GSNOR inhibitors may potentially serve as effective immunomodulators in both T cell- and B cell-mediated EAE and multiple sclerosis.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578673"},"PeriodicalIF":2.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471361","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 levels of tumor necrosis factor and TNFRSF1A gene polymorphisms in Egyptian multiple sclerosis patients: the influence on susceptibility and severity","authors":"Maged Abdel Naseer ,&nbsp;Montasser Hegazy ,&nbsp;Karim M. El-Mehdawy ,&nbsp;Hala Ashraf ,&nbsp;Ahmed Shawky ,&nbsp;Amr Mohamed Fouad","doi":"10.1016/j.jneuroim.2025.578672","DOIUrl":"10.1016/j.jneuroim.2025.578672","url":null,"abstract":"<div><h3>Introduction</h3><div>Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system that is caused by a complex interplay of genetic, epigenetic, and environmental factors.</div></div><div><h3>Objectives</h3><div>To investigate the relationship between serum levels of TNF and TNFRSF1A gene polymorphisms and their impact on the risk and severity of MS.</div></div><div><h3>Methods</h3><div>This case-control study included fifty patients with multiple sclerosis, both familial and non-familial, and fifty healthy matched controls. Molecular analysis of TNFRSF1A gene variants (rs1800693) was performed using TaqMan Real-Time PCR, and TNF serum levels were measured using ELISA.</div></div><div><h3>Results</h3><div>The frequency of the (C/C) genotype was significantly higher in patients (16 %) compared to controls (2 %). Additionally, the frequency of the (C) allele in TNFRSF1 (rs1800693) was significantly higher in patients (17 %) than in controls (2 %). The median serum TNF level was significantly higher in controls (79.99 Pg/ml, IQR: 67.39 to 434.48) compared to MS patients (67.93 Pg/ml, IQR: 57.15 to 80.79). Furthermore, the serum TNF level was significantly lower in patients with TNFSF1A gene variants C/C and C/T with a median of 56.31 Pg/ml (IQR: 48.84 to 73.9) compared to patients with TNFSF1A gene variant T/T with a median of 69.26 Pg/ml (IQR: 58.7 to 85.08). A significant negative correlation was found between serum TNF and EDSS in MS patients (<em>r</em> = −0.28, <em>p</em> value = 0.04).</div></div><div><h3>Conclusion</h3><div>The rs1800693 SNP (C/C) variant is a significant factor in the development of MS. Additionally, the reduced serum TNF levels observed in the carriers of the C allele may contribute to disease pathogenesis.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578672"},"PeriodicalIF":2.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322081","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":"A rare neuroendocrine presentation in pediatric anti-glutamic acid decarboxylase autoimmunity: Case report and literature review","authors":"Danilo de Assis Pereira ,&nbsp;Marina Mariano ,&nbsp;Nathalia Marcon ,&nbsp;Marianna Menezes Maia ,&nbsp;Mateus Mistieri Simabukuro ,&nbsp;Ana Carolina Coan ,&nbsp;Mariana Zorron","doi":"10.1016/j.jneuroim.2025.578670","DOIUrl":"10.1016/j.jneuroim.2025.578670","url":null,"abstract":"<div><div>Anti-glutamic acid decarboxylase (anti-GAD) antibodies are commonly associated with type 1 diabetes mellitus (T1DM) but can also indicate severe neurological involvement, including autoimmune encephalitis. We present the case of a previously healthy four-year-old girl who developed persistent focal epileptic seizures affecting the right hemiface, which progressed to epilepsia partialis continua and were accompanied by hyperglycemia and signs of premature thelarche. Additional findings included advanced bone age and a single episode of unexplained vaginal bleeding. Brain MRI and abdominal ultrasound were unremarkable, but EEG revealed left temporal spikes. Laboratory testing confirmed elevated anti-GAD antibodies (&gt;2000 IU/mL), supporting a diagnosis of autoimmune encephalitis. The patient was treated with intravenous immunoglobulin (IVIG), resulting in partial seizure control and improved glycemic regulation. This case underscores the need to consider autoimmune mechanisms in pediatric patients with pharmacoresistant seizures and concurrent endocrine abnormalities. Early identification of anti-GAD antibodies facilitated timely immunotherapy, emphasizing the value of integrated diagnostic and therapeutic strategies in managing rare autoimmune disorders.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578670"},"PeriodicalIF":2.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330581","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":"Prognostic significance of PD-L1 and CD45RO+ cells in glioblastoma: The modulating role of MMR status","authors":"Yousef Mohammadi ,&nbsp;Elina Kavini ,&nbsp;Simin Ahmadvand ,&nbsp;Amirreza Dehghanian ,&nbsp;Abbas Ghaderi","doi":"10.1016/j.jneuroim.2025.578669","DOIUrl":"10.1016/j.jneuroim.2025.578669","url":null,"abstract":"<div><h3>Background</h3><div>Glioblastoma (GBM) is the most prevalent and aggressive primary malignant brain tumor with limited treatment options and poor prognosis. Prognostic biomarkers, including immune checkpoint molecules and tumor-infiltrating lymphocytes, offer valuable insights into disease outcomes and potential therapeutic targets. This study uses Immunohistochemical analyses to explore the roles of PD-L1, CD45RO⁺ cells, and other key biomarkers in GBM prognosis.</div></div><div><h3>Methods</h3><div>Immunohistochemical (IHC) staining of PD-1, PD-L1, CD45RO, mismatch repair (MMR) proteins, and Ki-67 was conducted on 63 formalin-fixed paraffin-embedded (FFPE) GBM tissue samples. Statistical analyses, including Cox regression, assessed the prognostic impact of these biomarkers.</div></div><div><h3>Results</h3><div>IHC staining results indicated limited immune infiltration in the tumor tissue. High PD-L1 expression (HR: 1.926) and elevated CD45RO⁺ cells infiltration (HR: 2.122) were significantly associated with reduced OS in GBM patients. Subgroup analyses revealed that PD-L1 and CD45RO⁺ cells had a stronger prognostic impact in MMR-proficient patients, whereas IDH mutation status remained the only independent prognostic marker in MMR-deficient GBM cases.</div></div><div><h3>Conclusions</h3><div>PD-L1 and CD45RO⁺ cells serve as key prognostic biomarkers in GBM, particularly in MMR-proficient patients. These findings underscore the potential for personalized immunotherapies targeting immune checkpoint pathways to improve GBM outcomes. Further research is warranted to explore the therapeutic implications of these markers in GBM subgroups.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578669"},"PeriodicalIF":2.9,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306295","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":"Contribution of activated complements and CD59 to the pathophysiology of Rasmussen syndrome","authors":"Yukitoshi Takahashi ,&nbsp;Shigeko Nishimura ,&nbsp;Emiko Takao ,&nbsp;Risa Kasai ,&nbsp;Masataka Fukuoka ,&nbsp;Tokito Yamaguchi ,&nbsp;Yasukiyo Araki ,&nbsp;Chihiro Yonee ,&nbsp;Osamu Kawano ,&nbsp;Yoshiyuki Kondo ,&nbsp;Natsumi Saito ,&nbsp;Takefumi Higashijima ,&nbsp;Yasuko Kuroha ,&nbsp;Keisuke Watanabe ,&nbsp;Tamami Yano ,&nbsp;Hirofumi Kashii ,&nbsp;Kazunori Ogawa ,&nbsp;Kenichi Maeda ,&nbsp;Maasa Abe ,&nbsp;Misa Nakamura ,&nbsp;Yukiko Mogami","doi":"10.1016/j.jneuroim.2025.578667","DOIUrl":"10.1016/j.jneuroim.2025.578667","url":null,"abstract":"<div><div>Rasmussen syndrome (RS) is an autoimmune-associated epilepsy with refractory seizures and deteriorating motor and cognitive functions. We expect to unveil complex immunological pathophysiology from the viewpoint of complements to establish newer immunomodulatory treatments. We examined CSF levels of activated complements (iC3b, C5a and soluble membrane attack complex (sMAC)) and CD59 (inhibitor of MAC) using ELISA kits in 36 patients with RS and 44 disease controls (DCs). Disease duration from the onset of RS to CSF examination (mean ± SD) was 80.5 ± 89.7 months (<em>n</em> = 73). Seizure frequency at CSF examination was daily in 56, weekly in four, monthly in six, yearly in four and seizure-free in three CSF samples. The level of iC3b was significantly higher in RS than in DCs, but that of C5a, sMAC or CD59 was not different between RS and DCs. Levels of iC3b increased along with duration of disease. The ratio of patients with the levels of CD59 more than zero increased after the acute stage. Levels of CD59 in patients with daily seizure frequency were significantly lower than those with seizure control. The odds ratio between levels of CD59 and IVIg treatment by multiple linear regression analyses was significantly high. Maximum datum of activated complements or CD59 among the course of each patient was not related with final motor, cognitive and seizure outcomes. Reduction of CD59 may be one of crucial pathologies in the early stage of RS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578667"},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314058","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":"Platelet and immune cell crosstalk in dementia with Lewy bodies: Is there a unique inflammatory profile?","authors":"Noelia Arias ,&nbsp;Marc Boigues ,&nbsp;Lourdes Ispierto ,&nbsp;Dolores Vilas ,&nbsp;Ian Linares-Pardo ,&nbsp;Ramiro Álvarez ,&nbsp;Pau Pastor ,&nbsp;Marco A. Fernandez-Sanmartín ,&nbsp;Eva Martínez-Cáceres ,&nbsp;Katrin Beyer","doi":"10.1016/j.jneuroim.2025.578668","DOIUrl":"10.1016/j.jneuroim.2025.578668","url":null,"abstract":"<div><div>Neurodegenerative diseases such as dementia with Lewy bodies (DLB), Alzheimer's disease (AD), and Parkinson's disease (PD) share overlapping clinical features, making diagnosis challenging. This study evaluated hematological data from blood tests of DLB, AD and PD patients and control individuals, 16 each. The interaction between platelets and immune cells was analyzed using flow cytometry to identify disease-specific differences. DLB patients exhibited a non-significant trend toward lower absolute platelet counts and reduced percentages of total monocytes especially compared to AD. Monocyte–platelet interactions were associated with a significant increase of CD68 expression, which was more pronounced in DLB than in AD and PD. The CD68 receptor, a marker of monocyte and microglial activation and receptor for low-density lipoproteins (LDL), was significantly increased in DLB compared to both AD and PD. Based on CD68 expression, platelet count and CD14⁺ monocyte percentage, we developed two multiparametric logistic models to classify DLB patients from AD (AUC: 0.8095) and PD (AUC: 0.8056). After further validation, these differences may help distinguish DLB from AD and PD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"406 ","pages":"Article 578668"},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144296848","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}