Journal of neuroimmunology最新文献

{"title":"Sex-specific immune-biological profiles in Parkinson's disease","authors":"Roberta Bovenzi ,&nbsp;Matteo Conti ,&nbsp;Clara Simonetta ,&nbsp;Jacopo Bissacco ,&nbsp;Davide Mascioli ,&nbsp;Maria Mancini ,&nbsp;Veronica Buttarazzi ,&nbsp;Federica Veltri ,&nbsp;Giulia Maria Sancesario ,&nbsp;Silvio Bagetta ,&nbsp;Francesca D'Amaro ,&nbsp;Massimo Pieri ,&nbsp;Rocco Cerroni ,&nbsp;Claudio Liguori ,&nbsp;Valerio Chiurchiù ,&nbsp;Mariangela Pierantozzi ,&nbsp;Alessandro Stefani ,&nbsp;Nicola Biagio Mercuri ,&nbsp;Tommaso Schirinzi","doi":"10.1016/j.jneuroim.2025.578610","DOIUrl":"10.1016/j.jneuroim.2025.578610","url":null,"abstract":"<div><div>Depending on age, both the risk and characteristics of Parkinson's disease (PD) differ between the sexes. The immune system might have a role; however, human-based evidence remains scarce. Here, we investigated the relationship between peripheral immune cellular composition and the clinical-biological sexual dimorphism of PD. The leukocyte population count (neutrophils, lymphocytes, monocytes, eosinophils, and basophils), the neutrophil-to-lymphocyte ratio (NLR), and the monocytes-to-lymphocytes ratio (MLR) were collected and compared in 117 PD patients and 86 controls (CTLs), and then related to blood levels of sex hormones, CSF markers of neurodegeneration (α-synuclein, amyloid-β-42, amyloid-β-40, total tau, and phosphorylated-181-tau), and clinical features in male and female PD patients. Finally, a cluster analysis based on the three main leukocyte populations (neutrophils, lymphocytes, monocytes) was performed for the entire PD cohort. Male PD patients had lower lymphocyte counts and higher NLR than male CTLs. Females with PD had lower monocyte counts, NLR, and MLR than males with PD. Lymphocyte counts correlated with cognition in male, but not female, PD patients. Finally, two clusters of peripheral immune cellular composition were identified: the “high peripheral inflammation” one, mostly comprising male patients, with worse clinical features and greater central α-synuclein burden, and the “low peripheral inflammation cluster”, which mainly comprised female patients, with milder clinical features and lower central synucleinopathy. In conclusion, the peripheral immune pattern entails sex-specific clinical-biological profiles in PD. Moreover, systemic inflammation clusters with sex, sexual hormones, clinical features, and central synucleinopathy in PD, supporting the relevance of immunity in sexual dimorphism of the disease.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578610"},"PeriodicalIF":2.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143800372","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":"Clinical characteristics and immunotherapy efficacy in autoimmune-associated benign epilepsy with centrotemporal spikes: A prospective cohort study","authors":"Zhijie Zhang ,&nbsp;Jing Wu ,&nbsp;Danfeng Xu,&nbsp;Shengnan Zhao,&nbsp;Di Lian,&nbsp;Dandan Zhang,&nbsp;Ling Li","doi":"10.1016/j.jneuroim.2025.578603","DOIUrl":"10.1016/j.jneuroim.2025.578603","url":null,"abstract":"<div><h3>Introduction</h3><div>Benign Epilepsy with Centrotemporal Spikes (BECTS) is the most common form of focal epilepsy in pediatric patients. In clinical practice, immune dysregulation and neuroinflammation have been observed in a subset of patients with BECTS harboring latent Herpesviridae infections, including the Epstein-Barr Virus (EBV) and Human Cytomegalovirus (CMV). Therefore, the present study aimed to explore the correlation between clinical characteristics and immune dysregulation in autoimmunity-associated BECTS and latent viral or Mycoplasma infections.</div></div><div><h3>Method</h3><div>Fourteen pediatric patients diagnosed with autoimmunity-associated BECTS were prospectively enrolled and underwent assessment of their presentations and etiological and immunological indicators. Further, we evaluated the effectiveness and safety of specific immune therapies (intravenous methylprednisolone and/or intravenous immunoglobulin). Therapy efficacy was determined by a reduction in Rolandic spikes on electroencephalogram recordings and seizure frequency. Potential risk factors were assessed through a retrospective comparative analysis with a control group comprising 46 patients diagnosed with cryptogenic BECTS.</div></div><div><h3>Result</h3><div>The autoimmunity-associated BECTS cohort demonstrated a higher likelihood of cognitive impairment, ADHD, psychiatric symptoms, and atypical BECTS; required a greater number of anti-seizure medications (ASMs); and experienced longer delays from symptom onset to hospital admission. The prevalence of CMV infection was also found to be significantly higher in the autoimmune disease group than in the control group. Elevated levels of IL-6, IgG, and Complement C3 were observed in the sera of both infected and non-infected children with BECTS. Atypical BECTS and Bilateral Rolandic spikes in EEG were identified as key risk factors for autoimmunity-associated BECTS. Following immunotherapy (intravenous methylprednisolone and/or intravenous immunoglobulin), a substantial reduction in seizure frequency and accumulated spike-wave index (AccSWI) was observed.</div></div><div><h3>Conclusion</h3><div>These findings support the hypothesis that autoimmune mechanisms contribute to the pathogenesis of selected BECTS cases. Latent viral infections such as CMV may serve as potential triggers. Atypical presentations of BECTS, with Bilateral Rolandic spikes in EEG, indicate the possibility of an autoimmune-associated trigger. Immunotherapy appears to offer therapeutic benefits to patients with autoimmunity-associated BECTS.</div></div><div><h3>Clinical trial registration</h3><div>This single-center, longitudinal observational study (XH-16-029/<span><span>NCT02969213</span><svg><path></path></svg></span>) included pediatric patients diagnosed with epilepsy.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578603"},"PeriodicalIF":2.9,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807925","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":"Relapsing-remitting multiple sclerosis as a potential consequence of thalidomide treatment: A case report","authors":"Rodolfo Francisco Marques ,&nbsp;Denison Alves Pedrosa ,&nbsp;Natalia Talim ,&nbsp;Josemary Cavalcante Lemos ,&nbsp;Marco A. Lana-Peixoto","doi":"10.1016/j.jneuroim.2025.578606","DOIUrl":"10.1016/j.jneuroim.2025.578606","url":null,"abstract":"<div><div>We present the first reported case of central nervous system (CNS) demyelination associated with thalidomide. A 29-year-old female with a history of prurigo nodularis was prescribed thalidomide after the failure of other therapies. Three weeks later, she developed right hemiparesis and sensory disturbances in the right upper and lower extremities. Brain and spinal cord MRI showed hyperintense and gadolinium enhanced lesions. She was diagnosed with clinically isolated syndrome and treated with IV pulses of methylprednisolone with full recovery. Due to suspected association between her symptoms and thalidomide, the drug was discontinued. Three years later she returned to our Outpatient Clinic after being treated at another hospital for a new attack, characterized by muscle weakness and sensory disturbance in the lower limbs. Brain and spinal cord MRI showed new lesions, fulfilling the criteria for multiple sclerosis. We believe the association between thalidomide and CNS demyelination may be due to its tumor necrosis factor-α (TNF-α) inhibition effect. Biologic TNF-α inhibitors have been reported to cause CNS lesions, with cases of optic neuritis, transverse myelitis, multiple sclerosis, and neuromyelitis optica spectrum disorder developing after initiation of drugs such as etanercept, adalimumab, infliximab and golimumab. This report shows that thalidomide should be considered a potential cause of CNS demyelination, similar to biologic TNF-α inhibitors, and should be avoided in patients with a heightened risk.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578606"},"PeriodicalIF":2.9,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834662","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":"Rasmussen encephalitis and localized scleroderma of the lower limb: Another piece of the puzzle. A case-report and literature review with individual participant data","authors":"Adolfo Mazzeo ,&nbsp;Emanuele Cerulli Irelli ,&nbsp;Alessandra Morano ,&nbsp;Pierpaolo Quarato ,&nbsp;Giancarlo Di Gennaro ,&nbsp;Carlo Di Bonaventura","doi":"10.1016/j.jneuroim.2025.578608","DOIUrl":"10.1016/j.jneuroim.2025.578608","url":null,"abstract":"<div><div>The co-occurrence of Rasmussen encephalitis (RE) and localized scleroderma (LS) is rare and poorly known. We describe the unique case of a 23-year-old patient with late-onset RE of the right hemisphere, emerging 15 years following LS of the left lower limb exclusively.</div><div>Furthermore, through a systematic review of existing literature, we delineate distinct characteristics of RE concomitant with LS: a delayed onset compared to classical RE cases; its occurrence either preceding or succeeding LS; and the variable involvement of the ipsilateral or contralateral hemisphere to the affected craniofacial skin. These findings might provide some hints regarding the interplay between these two conditions.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578608"},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826396","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":"Nitric oxide and experimental autoimmune encephalomyelitis review","authors":"Maria Staykova,&nbsp;Anne Bruestle","doi":"10.1016/j.jneuroim.2025.578586","DOIUrl":"10.1016/j.jneuroim.2025.578586","url":null,"abstract":"<div><div>Immunisation with neuroantigen in complete Freund's adjuvant (CFA) results in a range from severe experimental autoimmune encephalomyelitis (EAE) to no EAE in various strains and sexes of rodents. When CFA was substituted for carbonyl iron, all were EAE-susceptible. One of the differences between the two adjuvants was the strong induction of inducible nitric oxide synthase in EAE-resistant strains by CFA.</div><div>The questions discussed in this review are:</div><div>1/ Could exaggerated production of nitric oxide protect against development of autoimmunity?</div><div>2/ Could non-susceptible strains be rendered susceptible to EAE by interfering with NO levels during the inductive phase?</div><div>3/ Could susceptible strains be rendered resistant to EAE by interfering with NO levels during the inductive phase?</div><div>The answer to the three questions is “yes” and one of the reasons is the NO-induced actin polarization in the encephalitogenic T cells leading to their reduced trans-endothelial migration.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578586"},"PeriodicalIF":2.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821176","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":"MOGAD optic neuritis after mild head/orbital trauma in six children","authors":"Alexander J. Sandweiss ,&nbsp;Jonathan Rosen ,&nbsp;Chaitanya Aduru ,&nbsp;Akansha Chandrasekar ,&nbsp;Kyla Blasingame ,&nbsp;Madhuri Chilakapati ,&nbsp;Rod Foroozan ,&nbsp;Jonathan M. Yarimi","doi":"10.1016/j.jneuroim.2025.578605","DOIUrl":"10.1016/j.jneuroim.2025.578605","url":null,"abstract":"<div><div>Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a potential cause of optic neuritis (ON). Its triggers and etiologies are not completely understood. We describe a novel clinical observation in six young patients with MOGAD-ON in the setting of strikingly parallel histories of mild head/orbital trauma. This is a single-center retrospective case series of six young patients and age-matched isolated MOGAD-ON controls. We present data both individually (de-identified, only the six trauma-associated cases) and in aggregate. Averages are presented as the arithmetic mean +/− SEM. 6/27 patients with MOGAD-ON, (3/6 female), between 8 and 18 years old presented with ON 5.5 days after mild head trauma. Four patients developed ON ipsilateral to their unilateral head trauma while two developed bilateral ON following midline head trauma. All patients tested positive for serum anti-MOG antibodies upon ON workup. They all received intravenous corticosteroids with rapid improvement in symptoms (5.5 weeks to full visual recovery) and none have since relapsed. No other patients with MOGAD-ON experienced preceding head trauma, and all patients in the control group were asked about trauma upon assessment of the history. Head trauma may serve as an inciting event in the presentation and diagnosis of MOGAD-ON. This novel observation provides a potential pathophysiologic mechanism independent of infectious triggers, although we cannot determine if these patients were already predisposed towards MOGAD-ON.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578605"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776380","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":"Glial changes in the dentate gyrus of neuronal-specific PTEN knockout mice correlate with changes in cell proliferation","authors":"Sarah E. Latchney ,&nbsp;Anjali C. Raheja ,&nbsp;Brayan R. Ruiz Lopez ,&nbsp;Paige D. Womble ,&nbsp;Katherine J. Blandin ,&nbsp;Joaquin N. Lugo","doi":"10.1016/j.jneuroim.2025.578604","DOIUrl":"10.1016/j.jneuroim.2025.578604","url":null,"abstract":"<div><div>Dysregulated hippocampal neurogenesis is a feature of temporal lobe epilepsy (TLE), marked by increased neuronal proliferation. The tumor suppressor gene phosphatase and tensin homolog (PTEN) regulates neuronal proliferation, and its deletion is implicated in TLE. We have previously shown that deletion of neuronal subset-specific (NS)-PTEN in mice increases the number of proliferating cells throughout the dentate gyrus, including subregions that are typically devoid of neurons but rich in glial cells, most notably the Hilus and Molecular Layer. In this study, we hypothesized that NS-PTEN knockout mice would exhibit increased numbers of microglia and astrocytes in these same dentate gyrus subregions. We performed immunohistochemistry for Iba1 (microglia) and GFAP (reactive astrocytes) on wild-type and NS-PTEN knockout mice at 4 and 10 weeks of age. Our data reveal that NS-PTEN knockout mice exhibit increased Iba1+ cell density at both ages, with some male-specific effects. Subregional analysis of the dentate gyrus showed that at 4 weeks, NS-PTEN knockout mice had greater Iba1+ cell density in the Granule Cell Layer (GCL) and Hilus, and at 10 weeks, increases were observed in the GCL, Hilus, and Molecular Layer. Additionally, we observed an increased number of microglia with an amoeboid morphology and fewer with thin, ramified processes. Contrast to Iba1+ microglia, GFAP+ reactive astrocytes were localized to the neurogenic GCL. Importantly, increases in both glial types strongly correlated with heightened cell proliferation (Ki67+ cells), as reported in our previous study, underscoring the role of glial cells in the spatial dysregulation of neurogenesis in NS-PTEN knockout mice.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578604"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783712","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":"Recurrent anti-NMDA receptor encephalitis in first-trimester pregnancy with initially antibody-negative CSF","authors":"Julia R. Jahansooz ,&nbsp;Alyssa M. Kameoka ,&nbsp;Jineane Shibuya ,&nbsp;Janette Abramowitz","doi":"10.1016/j.jneuroim.2025.578602","DOIUrl":"10.1016/j.jneuroim.2025.578602","url":null,"abstract":"<div><div>Anti-<em>N</em>-methyl-<span>d</span>-aspartate receptor (anti-NMDAR) encephalitis is a paraneoplastic autoimmune encephalomyelitis that predominantly affects females in their reproductive years <span><span>Dalmau et al., 2007</span></span> and <span><span>Dalmau et al., 2019</span></span>. It has been infrequently reported during pregnancy <span><span>Dono et al., 2023</span></span> and <span><span>Joubert et al., 2020</span></span>. We describe a case of a 25-year-old G4P2 patient at 11 weeks gestation with a history of anti-NMDAR encephalitis who presented with intermittent confusion for two weeks. Initial antibody tests for anti-NMDAR encephalitis in the cerebrospinal fluid (CSF) were negative. Repeat serum labs drawn upon readmission to the emergency department (ED) 3 weeks later were positive, and results were confirmed with repeat CSF testing. Following treatment, the patient returned to baseline and delivered a developmentally healthy, full-term baby. Current gold-standard testing for anti-NMDAR encephalitis is through detection of NMDAR antibodies in the CSF <span><span>Gresa-Arribas et al., 2014</span></span>. However, CSF antibody testing early in the disease course may not be as sensitive as traditionally thought, and repeat testing is indicated if high suspicion continues.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578602"},"PeriodicalIF":2.9,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768400","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":"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}