Journal of neuroimmunology最新文献

Immuno-deficient features of thymoma-associated myasthenia gravis patients with hypogammaglobulinemia: A condition comparable to Good's syndrome 胸腺瘤相关重症肌无力伴低γ -球蛋白血症患者的免疫缺陷特征：一种与古德综合征相当的病症。

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-05-01 Epub Date: 2026-02-05 DOI: 10.1016/j.jneuroim.2026.578885

Saki Nakashima , Kaori Sakuishi , Manato Hara , Reiko Kawasaki , Toshiyuki Kakumoto , Hiroyuki Ishiura , Tatsushi Toda

Good's syndrome (GS) is a rare immunodeficiency disorder associated with thymoma, characterized by hypogammaglobulinemia and recurrent infections; however, its clinical significance in thymoma-associated myasthenia gravis (TAMG) remains unclear. We retrospectively reviewed 30 patients with TAMG admitted to our center between January 2010 and March 2022. We defined GS-like immunodeficiency as serum IgG below the institutional cutoff of 861 mg/dL and a history of two or more infections requiring antimicrobial treatment; 11 patients (36.7%) met this definition. Compared with the remaining patients, the GS-like group had higher incidences of malignancy (45.5% vs. 5.3%, p = 0.016) and autoimmune diseases other than MG (36.4% vs. 5.3%, p = 0.047), lower peripheral lymphocyte counts (median 1100/μL vs. 2200/μL, p = 0.0051), and more frequent airflow obstruction defined by one second to forced vital capacity ratio of less than 70% (60.0% vs. 5.3%, p = 0.0026). Five deaths occurred in the GS-like group, and none in the other; median survival from the first antimicrobial-treated infection was 5.0 years. These findings imply that TAMG patients with GS-like immunodeficiency have a worse prognosis, underscoring the need for close monitoring and timely adjustments of MG management. (189 words).

古德氏综合征（GS）是一种罕见的与胸腺瘤相关的免疫缺陷疾病，以低γ球蛋白血症和复发性感染为特征；然而，其在胸腺瘤相关性重症肌无力（TAMG）中的临床意义尚不清楚。我们回顾性分析了2010年1月至2022年3月间本中心收治的30例tam患者。我们将gs样免疫缺陷定义为血清IgG低于861 mg/dL的法定临界值，并且有两次或两次以上需要抗菌药物治疗的感染史；11例患者（36.7%）符合此定义。与其他患者相比，gs样组的恶性肿瘤发生率（45.5% vs. 5.3%, p = 0.016）和MG以外的自身免疫性疾病发生率（36.4% vs. 5.3%, p = 0.047）较高，外周淋巴细胞计数较低（中位数1100/μL vs. 2200/μL, p = 0.0051），气流阻塞发生率较高（1秒与强迫肺活量之比小于70%）（60.0% vs. 5.3%, p = 0.0026）。gs样组有5例死亡，另一组无死亡；首次抗微生物药物治疗感染的中位生存期为5.0年。这些发现提示，伴有gs样免疫缺陷的tmg患者预后较差，强调密切监测和及时调整MG管理的必要性。(189字)。

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引用次数: 0

Possible risk of rheumatoid arthritis treated with methotrexate to the central nervous system relapse of diffuse large B-cell lymphoma 甲氨蝶呤治疗类风湿关节炎对弥漫性大b细胞淋巴瘤中枢神经系统复发的可能风险。

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-05-01 Epub Date: 2026-02-03 DOI: 10.1016/j.jneuroim.2026.578877

Rie Tabata , Hiroko Uesugi , Chiharu Tabata

Purpose

Relapse in the CNS is uncommon but often a fatal event in the patients with diffuse large B-cell lymphoma. An important management strategy consists of identifying patients in the high-risk group for CNS relapse and choosing those who will benefit from CNS prophylaxis. To evaluate rheumatoid arthritis as an additional risk factor for CNS relapse, we retrospectively examined the patients with DLBCL.

Methods

We examined 85 patients with diffuse large B-cell lymphoma, admitted to the hospital between June 2016 and May 2021 and followed up for at least three years, and investigate the background of nine patients with CNS relapse. CNS relapse was diagnosed by imaging, clinical, and histological or cytological findings. Also, we evaluated patients with a history of rheumatoid arthritis in these 85 patients. Statistical analysis was performed using Fisher's exact test (Statcel-the Useful Addin Forms on Excel-4th ed.)

Results

In the present study, we showed that nine of 85 patients (10.6%) developed CNS relapse. Three of nine cases with CNS relapse had none of the previously reported risks, but received low-dose methotrexate for rheumatoid arthritis. We observed a high proportion of CNS relapse among patients with diffuse large B-cell lymphoma and concomitant rheumatoid arthritis The association between CNS relapse and concomitant rheumatoid arthritis in diffuse large B-cell lymphoma was statistically significant. (CNS relapse / history of RA: +/+ 3, +/− 6, −/+ 5, −/− 71; p = 0.036), using Fisher's exact test.

Conclusions

Here we demonstrated a possible risk of rheumatoid arthritis for CNS relapse in diffuse large B-cell lymphoma. High-dose intravenous methotrexate has been increasingly used as a CNS prophylaxis instead of intrathecal methotrexate injection alone in patients with high-risk diffuse large B-cell lymphoma. However, our findings suggest that MTX re-administration in patients with rheumatoid arthritis with diffuse large B-cell lymphoma and high CNS relapse risk warrants particular caution.

Clinicians should be aware of the possible risks in these patients, and careful consideration is needed.

目的：弥漫性大b细胞淋巴瘤患者的中枢神经系统复发并不常见，但往往是致命的事件。一项重要的管理策略包括识别中枢神经系统复发的高危人群，并选择那些将受益于中枢神经系统预防的患者。为了评估类风湿关节炎作为中枢神经系统复发的另一个危险因素，我们回顾性检查了DLBCL患者。方法：对2016年6月至2021年5月收治的85例弥漫性大b细胞淋巴瘤患者进行随访，随访时间至少3年，并对其中9例中枢神经系统复发患者进行背景调查。中枢神经系统复发是通过影像学、临床和组织学或细胞学检查诊断的。此外，我们评估了这85例有类风湿关节炎病史的患者。统计学分析采用Fisher精确检验（statcel - Useful Addin Forms on excel -第4版）。结果：在本研究中，我们发现85例患者中有9例（10.6%）出现中枢神经系统复发。9例中枢神经系统复发病例中有3例没有先前报道的风险，但接受了低剂量甲氨蝶呤治疗类风湿性关节炎。我们观察到弥漫性大b细胞淋巴瘤合并类风湿关节炎患者的中枢神经系统复发比例很高，弥漫性大b细胞淋巴瘤患者中枢神经系统复发与合并类风湿关节炎的相关性具有统计学意义。（中枢神经系统复发/ RA病史：+/+ 3，+/- 6,-/+ 5,-/- 71;p = 0.036），采用Fisher精确检验。结论：本研究表明弥漫性大b细胞淋巴瘤患者中枢神经系统复发可能有类风湿关节炎的风险。高剂量静脉注射甲氨蝶呤已越来越多地用于高危弥漫性大b细胞淋巴瘤患者的中枢神经系统预防，而不是单独鞘内注射甲氨蝶呤。然而，我们的研究结果表明，类风湿关节炎弥漫性大b细胞淋巴瘤和中枢神经系统复发风险高的患者再次给予甲氨蝶呤需要特别谨慎。临床医生应该意识到这些患者可能存在的风险，并需要仔细考虑。

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引用次数: 0

Docosahexaenoic acid supplementation aggravates myasthenia gravis through immune dysregulation 二十二碳六烯酸通过免疫失调加重重症肌无力

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-05-01 Epub Date: 2026-02-10 DOI: 10.1016/j.jneuroim.2026.578889

Linqi Liu , Dan Lu , Wenjun Que , Rui Fan , Wei Zheng , Yaoqi Gan , Fei Xiao

Myasthenia gravis (MG) is an autoimmune disorder characterized by the disruption of immune cell homeostasis and inflammatory processes. However, the impact of metabolic abnormalities on immune regulation in MG has not been well defined. The objective of this study was to identify serum metabolites causally linked to MG and to explore their role in the onset and progression of the disease. This will provide a theoretical foundation for targeted clinical interventions and therapeutic strategies. To establish the causal relationship between serum metabolites and MG, we employed Mendelian randomization. Furthermore, we conducted dietary interventions with docosahexaenoic acid (DHA) to observe its effects on the disease progression and immune cell subpopulations in experimental autoimmune myasthenia gravis (EAMG) rats. We also performed metabolomic and transcriptomic analyses of regulatory T cells (Treg) during MG progression. Our findings suggest that dysregulated lipid metabolism, particularly elevated DHA levels, is a significant risk factor for MG, influencing various markers associated with Treg cells in both MG patients and in EAMG models. The addition of 1% DHA to the diet exacerbated the severity of EAMG, enhanced B cell immune responses, and promoted antibody production. However, it also led to an increase in the proportion of Treg cells. Further in vitro experiments confirmed that DHA accumulation in Treg cells enhances their proliferation but impairs their inhibitory function, partially through the PI3K-Akt signaling pathway. These results imply that modulating lipid metabolism, especially through the PI3K-Akt pathway in Treg cells, could be critical in controlling MG.

重症肌无力（MG）是一种自身免疫性疾病，其特征是免疫细胞稳态和炎症过程的破坏。然而，代谢异常对MG免疫调节的影响尚未明确。本研究的目的是确定与MG有因果关系的血清代谢物，并探讨它们在疾病发生和进展中的作用。这将为有针对性的临床干预和治疗策略提供理论基础。为了建立血清代谢物与MG之间的因果关系，我们采用孟德尔随机化。此外，我们对实验性自身免疫性重症肌无力（EAMG）大鼠进行二十二碳六烯酸（DHA）饮食干预，观察其对疾病进展和免疫细胞亚群的影响。我们还对MG进展过程中的调节性T细胞（Treg）进行了代谢组学和转录组学分析。我们的研究结果表明，脂质代谢失调，特别是DHA水平升高，是MG的重要危险因素，影响MG患者和EAMG模型中与Treg细胞相关的各种标志物。饲料中添加1% DHA可加重EAMG的严重程度，增强B细胞免疫反应，促进抗体产生。然而，它也导致Treg细胞比例的增加。进一步的体外实验证实，DHA在Treg细胞中的积累增强了其增殖，但损害了其抑制功能，部分是通过PI3K-Akt信号通路实现的。这些结果表明，调节脂质代谢，特别是通过Treg细胞中的PI3K-Akt通路，可能是控制MG的关键。

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引用次数: 0

Longitudinal MuSK antibody levels may correlate with disease severity in MuSK myasthenia gravis 麝香纵向抗体水平可能与麝香型重症肌无力的疾病严重程度相关。

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-05-01 Epub Date: 2026-02-01 DOI: 10.1016/j.jneuroim.2026.578876

Manato Yasuda , Akiyuki Uzawa , Etsuko Ogaya , Hideo Handa , Kentaro Kurumada , Kyosuke Takasaka , Hiroyuki Akamine , Yukiko Ozawa , Satoshi Kuwabara

Background

In muscle-specific kinase antibody-positive myasthenia gravis (MuSK-MG), the clinical utility of MuSK antibody levels as a biomarker for disease severity is debated, with conflicting reports on its correlation with clinical status. This study aimed to clarify this association by applying a rigorous statistical model to a longitudinal dataset followed from an immunotherapy-naïve state.

Methods

We conducted a retrospective longitudinal study on 6 patients with MuSK-MG tracked from their treatment-naïve baseline. The primary analysis used 103 data points where MuSK antibody levels and MG activities of daily living (MG-ADL) scores were available. A secondary analysis used the subset of 81 data points where total immunoglobulin G (IgG) levels were also concurrently measured. Generalized linear mixed-effects models (GLMM) were used to assess the intrapatient correlation, adjusting for interpatient variability by including a random intercept for each subject.

Results

First, the GLMM analysis of 103 data points revealed a strong positive intrapatient correlation between MuSK antibody levels and MG-ADL scores (P < 0.001). Second, in the subset analysis (n = 81), MuSK antibody levels remained positively and specifically correlated with MG-ADL scores (P = 0.002), whereas total IgG levels showed no independent correlation (P = 0.61) when included in the same model.

Conclusions

MuSK antibody level, unlike total IgG, is a specific and valuable biomarker for monitoring intrapatient disease activity and therapeutic response. These findings strongly support the utility of serial MuSK antibody monitoring within individual patients.

背景：在肌肉特异性激酶抗体阳性的重症肌无力（MuSK- mg）中，MuSK抗体水平作为疾病严重程度的生物标志物的临床应用存在争议，关于其与临床状态的相关性的报道相互矛盾。本研究旨在通过应用严格的统计模型来澄清这种关联，以纵向数据集遵循immunotherapy-naïve状态。方法：我们对6例MuSK-MG患者进行了回顾性的纵向研究，追踪他们的treatment-naïve基线。初步分析使用103个数据点，其中MuSK抗体水平和MG日常生活活性（MG- adl）评分可用。第二次分析使用了81个数据点的子集，其中也同时测量了总免疫球蛋白G （IgG）水平。使用广义线性混合效应模型（GLMM）来评估患者内部相关性，通过包括每个受试者的随机截距来调整患者间变异性。结果：首先，103个数据点的GLMM分析显示，MuSK抗体水平与MG-ADL评分之间存在很强的正相关性(P)。结论：MuSK抗体水平与总IgG不同，是监测患者体内疾病活动和治疗反应的特异性和有价值的生物标志物。这些发现有力地支持了对个体患者进行MuSK抗体连续监测的实用性。

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引用次数: 0

Effect of pharmacological intervention and pathogenesis discussion about rats with tic disorders 抽动障碍大鼠的药理干预作用及发病机制探讨

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-05-01 Epub Date: 2026-02-05 DOI: 10.1016/j.jneuroim.2026.578878

Xiaofang Liu , Xiaohong Jiang , Zijia Chen , Xiaona Xue , Sumei Wang , Lvping Lin

To investigate the pathogenesis of Tic disorders (TD), particularly their relationship with central nervous system inflammation, we conducted an animal experiment. A TD model was established for rats, and their behavior and immune cytokines and receptor in the striatum were compared between a diseased group and healthy control group of rats. After receiving effective drug interventions (the traditional Chinese medicine Jian-Pi-Zhi-Dong decoction (JPZDD) and the Western medicine Tiapride), we observed changes in behavior and immune cytokine and receptor expression in the striatum and analyzed the association between central nervous system inflammation and TD. The results are as follows: (1) Successful modeling: Compared to normal rats, TD diseased rats exhibited increased spontaneous activity, stereotypical exercise, and elevated expression of inflammatory cytokines and receptor in the striatum. (2) Effective pharmacological intervention: Tiapride and JPZDD reduced spontaneous activity, stereotypical exercise, and the expression of inflammatory cytokines and receptor in rats with TD. (3) The number of spontaneous activities and stereotypical exercise scores was positively correlated with central nervous system inflammation. The expression of Toll-like receptor 4 (TLR4), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) in the striatum of the diseased group rats were significantly greater than those in the striatum of the normal group rats. Effective pharmacological intervention reduced the expression of inflammatory cytokine and receptor in the striatum, bringing them to expression similar to those in normal rats. Based on these results, we conclude that TD is associated with central nervous system inflammation and that the severity of TD is positively correlated with the severity of central nervous system inflammation. We hypothesize that the pathogenesis of TD may involve elevated TLR4, which triggers overactivation of microglia in the brain resulting in the release of excessive IL-6, IL-8, and TNF-α. This process damages neurons and leads to tic symptoms in patients.

为了探讨抽动障碍（TD）的发病机制，特别是其与中枢神经系统炎症的关系，我们进行了动物实验。建立大鼠TD模型，比较患病组和健康对照组大鼠行为及纹状体免疫细胞因子和受体。在接受有效药物干预（中药健脾治洞汤和西药硫必利）后，观察纹状体行为和免疫细胞因子及受体表达的变化，分析中枢神经系统炎症与TD的关系。结果如下：(1)成功造模：与正常大鼠相比，TD病鼠自发性活动增加，典型运动增加，纹状体炎症细胞因子和受体表达升高。(2)有效的药物干预：Tiapride和JPZDD降低了TD大鼠的自发活动、刻板运动以及炎症因子和受体的表达。(3)自发性活动次数和定型运动得分与中枢神经系统炎症呈正相关。病变组大鼠纹状体中toll样受体4 （TLR4）、白细胞介素-6 （IL-6）、白细胞介素-8 （IL-8）、肿瘤坏死因子-α (TNF-α)的表达均显著高于正常组大鼠。有效的药物干预降低了纹状体中炎症细胞因子和受体的表达，使其表达与正常大鼠相似。基于这些结果，我们认为TD与中枢神经系统炎症有关，并且TD的严重程度与中枢神经系统炎症的严重程度呈正相关。我们假设TD的发病机制可能与TLR4升高有关，TLR4升高触发脑内小胶质细胞过度激活，导致过量IL-6、IL-8和TNF-α的释放。这一过程会损害神经元，导致患者出现抽动症状。

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引用次数: 0

Bilateral optic neuritis preceding a Baló concentric sclerosis lesion: A case report and literature review 双侧视神经炎前Baló同心硬化病变：1例报告及文献复习

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-04-01 Epub Date: 2026-01-27 DOI: 10.1016/j.jneuroim.2026.578874

David F. Alfonso-Cedeño , Lorena Medina-Lozano , Paula V. Gaete , Patricia Quintero-Cusguen

Baló's concentric sclerosis (BCS) is a rare inflammatory demyelinating disorder characterised by a pathologic appearance of concentric layers of demyelinated and partially myelinated fibres, with a distinctive “onion bulb” pattern on magnetic resonance imaging (MRI). Due to its rarity and overlapping features with multiple sclerosis and neuromyelitis optica spectrum disorder (NMOSD), diagnosis is challenging. We report the case of a 60-year-old male with hypertension who presented with acute bilateral painless vision loss, absent pupillary light reflex, and marked photophobia. Initial brain and orbital MRI were normal, but cervical spine MRI revealed a demyelinating lesion from C5 to C6. Cerebrospinal fluid (CSF) showed type 1 oligoclonal bands and negative anti-aquaporin 4 and anti-myelin oligodendrocyte glycoprotein antibodies. The patient was initially diagnosed with seronegative NMOSD and treated with intravenous methylprednisolone without improvement. One month later, he developed spastic dysarthria and dysphagia; brain MRI showed a right pre-Rolandic lesion with concentric rings associated with the previously reported demyelinated lesion in the cervical spinal cord and other demyelinated lesions in the brainstem. CSF analysis during relapse revealed hyperproteinorrhachia and mild hypoglycorrhachia without infectious or autoimmune markers. Plasmapheresis led to the resolution of bulbar symptoms. Given clinical relapse and lesion progression, rituximab therapy was initiated, achieving clinical stability. This case illustrates the diagnostic complexity of BCS, the importance of integrating imaging and immunological findings, and the potential role of B-cell–depleting therapy in preventing new relapses.

Baló的同心圆硬化（BCS）是一种罕见的炎症性脱髓鞘疾病，其病理特征是脱髓鞘和部分髓鞘纤维的同心圆层，在磁共振成像（MRI）上具有独特的“洋葱球”模式。由于其罕见性和与多发性硬化症和视神经脊髓炎频谱障碍（NMOSD）重叠的特征，诊断具有挑战性。我们报告一例60岁男性高血压患者，其表现为急性双侧无痛性视力丧失，瞳孔光反射缺失，以及明显的畏光。最初的脑部和眼眶MRI正常，但颈椎MRI显示C5至C6处脱髓鞘病变。脑脊液（CSF）显示1型寡克隆带，抗水通道蛋白4和抗髓鞘少突胶质细胞糖蛋白抗体阴性。患者最初被诊断为血清阴性NMOSD，并静脉注射甲基强的松龙治疗，但没有改善。1个月后出现痉挛性构音障碍和吞咽困难；脑MRI显示右侧rolandic前病变伴同心圆，与先前报道的颈脊髓脱髓鞘病变和脑干其他脱髓鞘病变相关。复发期间的脑脊液分析显示高蛋白血症和轻度低糖血症，无感染性或自身免疫性标志物。血浆置换导致了球症状的缓解。鉴于临床复发和病变进展，开始使用利妥昔单抗治疗，达到临床稳定。该病例说明了BCS诊断的复杂性，影像学和免疫学检查的重要性，以及b细胞消耗治疗在预防新复发中的潜在作用。

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引用次数: 0

Efgartigimod for steroid-resistant autoimmune glial fibrillary acidic protein astrocytopathy: a case report and literature review 依加替莫德治疗类固醇抵抗性自身免疫性胶质原纤维酸性蛋白星形细胞病1例报告并文献复习

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-04-01 Epub Date: 2026-01-24 DOI: 10.1016/j.jneuroim.2026.578866

Peng Lei , Yun Lu , Jie Xia , Tao Wang , Ling Zhong

Background

Neonatal Fc receptor (FcRn) inhibitors rapidly and specifically clear serum immunoglobulin G (IgG) levels and, therefore, are increasingly used for the treatment of neurological autoimmune diseases, such as myasthenia gravis. However, whether FcRn inhibitors could alleviate steroid-unresponsive glial fibrillary acidic protein astrocytopathy (GFAP-A) has not been reported.

Case presentation

We report a case of a 68-year-old male patient who presented with gait instability and numbness in the left hand. Cranial magnetic resonance imaging (MRI) revealed multiple demyelinating lesions. The initial clinical diagnosis was demyelinating encephalopathy. After 1 month of intravenous methylprednisolone pulse therapy, followed by sequential oral prednisone, the patient's gait instability did not improve. Upon re-examination at our hospital, cranial MRI revealed no significant changes in the lesions. Testing for central nervous system demyelinating antibodies revealed serum anti-GFAP IgG antibody (titer 1:100), cerebrospinal fluid anti-GFAP IgG antibody (titer 1:1), and negative result for oligoclonal bands in blood and the cerebrospinal fluid. The final diagnosis was GFAP-A. Treatment with the FcRn inhibitor efgartigimod significantly improved clinical symptoms and brain lesions.

Conclusions

This rare case indicates that efgartigimod is a promising treatment option for steroid-unresponsive GFAP-A.

背景：新生儿Fc受体（FcRn）抑制剂可快速特异性清除血清免疫球蛋白G （IgG）水平，因此越来越多地用于治疗神经自身免疫性疾病，如重症肌无力。然而，FcRn抑制剂是否可以缓解类固醇无反应的胶质原纤维酸性蛋白星形细胞病（GFAP-A）尚未报道。我们报告一例68岁男性患者，其表现为步态不稳和左手麻木。头颅磁共振成像（MRI）显示多发脱髓鞘病变。最初的临床诊断为脱髓鞘性脑病。静脉注射甲基强的松龙脉冲治疗1个月后，随后连续口服强的松，患者的步态不稳定没有改善。在我院复查后，颅脑MRI显示病变无明显变化。中枢神经系统脱髓鞘抗体检测血清抗gfap IgG抗体（滴度1:100），脑脊液抗gfap IgG抗体（滴度1:1），血、脑脊液寡克隆带阴性。最终诊断为gmap - a。使用FcRn抑制剂efgartigimod治疗可显著改善临床症状和脑部病变。结论这一罕见的病例表明依加替莫德是治疗类固醇无反应的GFAP-A的一种有希望的治疗选择。

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引用次数: 0

Exercise ameliorates microglial activation and cognitive impairment induced by GFAT1 knockdown after traumatic brain injury 运动可改善创伤性脑损伤后GFAT1敲低引起的小胶质细胞激活和认知障碍

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-04-01 Epub Date: 2026-01-13 DOI: 10.1016/j.jneuroim.2026.578868

Tianyu Zai , Mengqi Liu , Weiguan Chen , Chengwei Duan , Jiahao Zhang , Baohao Zheng , Hongjian Lu

Background

The potential of exercise to prevent traumatic brain injury (TBI) has been extensively studied. Microglia play a critical role in TBI pathogenesis. Glutamine-fructose-6-phosphate transaminase 1 (GFAT1), the key enzyme regulating the hexosamine biosynthetic pathway (HBP), not only controls glucose influx but also plays an important role in the neuroinflammatory process. However, the relationship between GFAT1 expression and microglial metabolic activity during treadmill exercise in TBI mice remains unclear.

Methods

A mouse TBI model was established via needle puncture, with mice randomly divided into sedentary and 14-day voluntary treadmill-running exercise groups. GFAT1 knockdown was achieved using GFAT1 shRNA lentivirus. Behavioral tests, electrophysiological recordings, immunohistochemistry, immunofluorescence, and Western blotting evaluated microglial activation and neurological function. An in vitro cell model was constructed with irisin and LPS, using Western blotting and TUNEL staining to assess inflammatory proteins and neuronal apoptosis.

Results

The TBI group showed higher GFAT1 expression than the sham group. Following TBI induction, GFAT1 knockdown increased Interleukin-6(IL-6) expression and aggravate cognitive impairment. While exercise training promoted cognitive function recovery, reduced IL-6 expression, and upregulated the expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). In vitro LPS stimulation induced the expression of GFAT1, IL-6, and iNOS; however, GFAT1 knockdown further exacerbated the expression of IL-6 and iNOS. Furthermore, irisin pretreatment led to a reduction in neuronal apoptosis, an increase in Nrf2 and HO-1 expression, and a decrease in IL-6 and iNOS expression.

Conclusion

Exercise ameliorates microglial activation and cognitive impairment induced by GFAT1 knockdown after traumatic brain injury.

运动预防创伤性脑损伤（TBI）的潜力已经得到了广泛的研究。小胶质细胞在TBI发病中起关键作用。谷氨酰胺-果糖-6-磷酸转氨酶1 （GFAT1）是调节己糖胺生物合成途径（HBP）的关键酶，不仅控制葡萄糖内流，而且在神经炎症过程中发挥重要作用。然而，GFAT1表达与TBI小鼠在跑步机运动中小胶质细胞代谢活性之间的关系尚不清楚。方法采用针刺法建立小鼠脑损伤模型，将小鼠随机分为久坐组和14 d自愿跑步组。利用GFAT1 shRNA慢病毒实现了GFAT1的敲除。行为测试、电生理记录、免疫组织化学、免疫荧光和Western blotting评估小胶质细胞激活和神经功能。用鸢尾素和LPS构建体外细胞模型，采用Western blotting和TUNEL染色检测炎症蛋白和神经元凋亡。结果脑外伤组GFAT1表达明显高于假手术组。TBI诱导后，GFAT1敲低可增加白细胞介素-6（IL-6）的表达，加重认知障碍。运动训练促进认知功能恢复，降低IL-6表达，上调核因子e2相关因子2 （Nrf2）和血红素加氧酶-1 （HO-1）表达。体外LPS刺激诱导GFAT1、IL-6和iNOS的表达；而GFAT1敲低进一步加剧了IL-6和iNOS的表达。此外，鸢尾素预处理导致神经元凋亡减少，Nrf2和HO-1表达增加，IL-6和iNOS表达降低。结论运动可改善创伤性脑损伤后GFAT1敲低引起的小胶质细胞活化和认知功能障碍。

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引用次数: 0

Brain tumor detection using HyGSNet and feature extraction with DWT-based GDP 基于HyGSNet的脑肿瘤检测和基于dwt的GDP特征提取。

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-04-01 Epub Date: 2026-01-14 DOI: 10.1016/j.jneuroim.2026.578869

Ponlatha Sambandham , Someswari Perla , Katakam Venkateswara Rao , Ganji Ramanjaiah

A life-threatening condition that impacts neurological function is brain tumors, which can lead to psychiatric complications such as depression and panic attacks. Timely and accurate detection, followed by appropriate treatment, is essential to improve the quality of life. Quick and early recognition of brain tumors significantly enhances treatment outcomes and promotes effective healing. In this context, medical image processing plays a critical role in assisting clinicians to detect and classify brain abnormalities. However, the manual process is time-consuming and heavily reliant on the expertise of physicians. Therefore, an intelligent system for brain tumor detection is essential to support clinical decision-making. This research presented a Hybrid Google SpinalNet (HyGSNet) to automatically detect brain tumors from Magnetic resonance imaging (MRI) images. Here, the proposed HyGSNet model is the hybridization of GoogleNet and SpinalNet. Initially, the Adaptive Wiener filter is used for pre-processing the input image, and the UNeXt is used for the segmentation of the filtered image. Then, the image augmentation process is followed by feature extraction to extract the essential features. Finally, the extracted features are passed to the HyGSNet for detecting brain tumor. Here, the performance of HyGSNet is evaluated with various evaluation metrics. The HyGSNet approach recorded high performance with specificity of 93%, accuracy of 93%, and sensitivity of 93.7%. The experimental results demonstrate that the proposed approach achieves consistently high performance across key evaluation metrics, indicating its robustness and reliability for brain tumor detection.

脑肿瘤是一种影响神经功能的危及生命的疾病，它会导致精神并发症，如抑郁和恐慌发作。及时准确的检测，然后进行适当的治疗，对于提高生活质量至关重要。快速和早期识别脑肿瘤可显著提高治疗效果并促进有效愈合。在这种情况下，医学图像处理在帮助临床医生检测和分类大脑异常方面起着至关重要的作用。然而，手工过程非常耗时，并且严重依赖于医生的专业知识。因此，一个智能的脑肿瘤检测系统是支持临床决策的必要条件。本研究提出了一种混合谷歌SpinalNet (HyGSNet)，用于从磁共振成像（MRI）图像中自动检测脑肿瘤。在这里，提出的HyGSNet模型是GoogleNet和SpinalNet的杂交。首先使用自适应维纳滤波器对输入图像进行预处理，然后使用UNeXt对滤波后的图像进行分割。然后，对图像进行增强处理，然后进行特征提取，提取基本特征。最后，将提取的特征传递给HyGSNet进行脑肿瘤检测。在这里，HyGSNet的性能用各种评估指标进行评估。HyGSNet方法的特异度为93%，准确度为93%，灵敏度为93.7%。实验结果表明，该方法在关键评价指标上均取得了一致的高性能，表明了该方法对脑肿瘤检测的鲁棒性和可靠性。

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引用次数: 0

Postbiotics and the gut–brain axis: A mechanistic review on modulating neuroinflammation and cognitive aging 后生物与肠-脑轴：调节神经炎症和认知衰老的机制综述。

IF 2.5 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2026-04-01 Epub Date: 2026-01-19 DOI: 10.1016/j.jneuroim.2026.578870

Rijhul Lahariya , Gargee Anand , Bandana Kumari , Ketan Priyadarshi

Aging triggers gut microbiota dysbiosis that disrupts the gut-brain axis (GBA), promoting neuroinflammation and neurodegeneration. Elderly exhibit reduced microbial diversity, depleted beneficial bacteria, and expanded pathobionts, elevating neurotoxic metabolites—lipopolysaccharides (LPS), trimethylamine-N-oxide, kynurenine derivatives, and secondary bile acids. These drive “inflammaging,” blood-brain barrier breakdown, microglial activation, mitochondrial impairment, and proteinopathies in Alzheimer's and Parkinson's disease. Conversely, neuroprotective metabolites from commensals—short-chain fatty acids, indole-3-propionic acid, and urolithins—preserve gut integrity, suppress inflammation, upregulate BDNF for synaptic plasticity, and enhance mitophagy. Postbiotics, stable probiotic-derived bioactives (butyrate, polyphenol metabolites, and lactate derivatives), surpass live probiotics in safety and precision. They modulate GBA via histone deacetylase inhibition, GPR41/43 signaling, NF-κB blockade, and microglial M2 shift, blocking LPS translocation and bolstering neuronal resilience. Preclinical rodent studies demonstrate robust neuroprotection, but human translation reveals challenges: inter-individual microbiota variability (diet/genetics/comorbidities), inconsistent metabolite absorption/brain penetration between species, methodological limitations (16S rRNA vs. functional metagenomics), postbiotic standardization barriers, and sparse Phase I/II trials showing biomarker benefits without cognitive endpoints. This review synthesizes gut dysbiosis-metabolite-brain aging mechanisms, positioning postbiotics as precision therapeutics. Multi-omics stratified controlled trials are essential to validate long-term efficacy for delaying neurodegeneration and extending cognitive health.

衰老会引发肠道菌群失调，破坏肠脑轴（GBA），促进神经炎症和神经变性。老年人表现出微生物多样性减少，有益菌减少，病原体增加，神经毒性代谢物-脂多糖（LPS），三甲胺- n -氧化物，犬尿氨酸衍生物和次级胆汁酸升高。这些会导致“炎症”、血脑屏障破裂、小胶质细胞激活、线粒体损伤以及阿尔茨海默氏症和帕金森病中的蛋白质病变。相反，来自评论体的神经保护代谢产物——短链脂肪酸、吲哚-3-丙酸和尿石素——保护肠道完整性，抑制炎症，上调BDNF以促进突触可塑性，并增强线粒体自噬。后益生菌，稳定的益生菌衍生的生物活性物质（丁酸盐、多酚代谢物和乳酸衍生物），在安全性和精确度上超过了活的益生菌。它们通过组蛋白去乙酰化酶抑制、GPR41/43信号传导、NF-κB阻断和小胶质M2移位来调节GBA，从而阻断LPS易位并增强神经元的弹性。临床前啮齿动物研究显示了强大的神经保护作用，但人类翻译显示了挑战：个体间微生物群的可变性（饮食/遗传/合共病），物种间代谢物吸收/脑渗透不一致，方法局限性（16S rRNA与功能宏基因组学），生物后标准化障碍，以及缺乏认知终点的生物标志物益处的稀疏I/II期试验。这篇综述综合了肠道生态失调-代谢-脑老化机制，定位后生物作为精确治疗。多组学分层对照试验对于验证延缓神经变性和延长认知健康的长期疗效至关重要。

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引用次数: 0