Clinical and Experimental Neuroimmunology最新文献

{"title":"Muscle magnetic resonance imaging findings in patients with idiopathic inflammatory myopathies","authors":"Tadanori Hamano,&nbsp;Tomoko Kamisawa,&nbsp;Sayaka Sanada,&nbsp;Kouji Hayashi","doi":"10.1111/cen3.12831","DOIUrl":"https://doi.org/10.1111/cen3.12831","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Idiopathic inflammatory myopathies (IIMs) are disorders that cause chronic muscle inflammation and weakness due to an autoimmune pathogenesis. Dermatomyositis (DM) is a typical IIM disorder, along with others including antisynthetic syndrome (ASS), immune-mediated necrotizing myopathy (IMNM), overlap myositis, inclusion body myositis (IBM), and anti-mitochondrial M2 antibody-positive myositis (AMA-myositis). Noninvasive muscle magnetic resonance imaging (MRI) is useful for determining the distribution, nature, and extent of lesions in affected muscles. T₁-weighted MRI is useful for observing morphological changes, including muscle atrophy. Short tau inversion recovery images or T₂-weighted images are useful for detecting muscle inflammation and edema and are suitable for selecting optimal biopsy sites. Muscle MRI is also useful for follow-up studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>On muscle MRI, patients with DM show a symmetric pattern with prominent fasciitis. The MRI findings in ASS are similar to those in DM. In IMNM, MRI findings are asymmetric, present a rapid and severe course, and fasciitis is less prominent. In IBM, atrophy is more severe at presentation than in other IIMs, and fasciitis is absent. In AMA-myositis, fasciitis is severe and atrophy is mild.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Muscle MRI can help differentiate between IIMs along with using other laboratory findings, including myositis-specific antibodies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"72-83"},"PeriodicalIF":0.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12831","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferons in myositis: Pathogenesis and therapy","authors":"Nozomu Tawara","doi":"10.1111/cen3.12827","DOIUrl":"https://doi.org/10.1111/cen3.12827","url":null,"abstract":"<p>Idiopathic inflammatory myopathies (IIMs), or myositis, are a heterogeneous group of autoimmune diseases affecting skeletal muscle and other organs. Recent research has revealed the important role of interferons (IFNs) in the pathogenesis of IIMs. This review summarizes the three types of IFNs and their functions in the immune system, focusing on their association with different IIM subtypes. Dermatomyositis (DM) is strongly associated with Type I IFNs. In contrast, inclusion body myositis (IBM), polymyositis with mitochondrial pathology (PM-mito), and anti-synthetase syndrome (ASyS) are predominantly associated with Type II IFN. This review explores the molecular mechanisms underlying these associations and their impact on muscle function. In addition, the potential of the IFN signaling pathway as a therapeutic target for IIMs will be discussed. Several clinical trials are currently underway or planned that target the IFN pathway using JAK inhibitors and monoclonal antibodies against Type I IFNs. JAK inhibitors have shown promise in treating DM, particularly in refractory cases. However, more research is needed to fully understand their efficacy and safety profiles in IIMs. The review concludes by highlighting the importance of ongoing research in this area and the potential for new targeted therapies in treating IIMs.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"64-71"},"PeriodicalIF":0.0,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant expression of long noncoding RNAs regulates inflammasome activation via oxidative stress: A novel mechanism for neuroinflammation and neurodegeneration in Parkinson's disease","authors":"Irene Mary Praveen,&nbsp;Latchoumycandane Calivarathan","doi":"10.1111/cen3.12830","DOIUrl":"https://doi.org/10.1111/cen3.12830","url":null,"abstract":"<p>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to hallmark motor symptoms such as bradykinesia, tremors, and rigidity. Emerging evidence suggests that the dysregulation or aberrant expression of long noncoding RNAs (lncRNAs) plays a critical role in the pathogenesis of PD by activating the inflammasome, either directly or via oxidative stress. Aberrant lncRNA expression has been linked to alterations in genes related to oxidative stress, causing an imbalance between reactive oxygen species (ROS) and antioxidant defenses. This imbalance contributes to mitochondrial dysfunction and neuronal damage. The NLRP3 inflammasome is a multiprotein complex comprising a sensor protein (eg, NLRP3), an adaptor protein (ASC), and an effector protein (caspase-1). Its activation involves priming via NF-κB signaling and is triggered by ROS, mitochondrial dysfunction, death-associated molecular patterns, or extracellular ATP. Once activated, the inflammasome promotes the cleavage and maturation of the proinflammatory cytokines IL-1β and IL-18, amplifying neuroinflammation and leading to neurodegeneration in PD. Crosstalk between dysregulated lncRNAs, ROS production, and inflammasome activation creates a vicious cycle of neuroinflammation and neurodegeneration, exacerbating PD progression. This review explores the molecular mechanisms linking lncRNA dysregulation to inflammasome activation in PD, either directly or through oxidative stress. It also highlights key lncRNAs involved in these processes. Furthermore, potential therapeutic strategies targeting these pathways, such as antioxidants, lncRNA modulators, and inflammasome inhibitors, offer promising avenues to mitigate neuroinflammation and slow neurodegeneration in PD.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"237-253"},"PeriodicalIF":0.0,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unmasking the muscle mysteries: Cutting-edge insights into inflammatory myopathies","authors":"Satoshi Yamashita","doi":"10.1111/cen3.12826","DOIUrl":"https://doi.org/10.1111/cen3.12826","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"42-43"},"PeriodicalIF":0.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Update on pathology of inflammatory myopathy","authors":"Akinori Uruha,&nbsp;Satoko Uruha","doi":"10.1111/cen3.12824","DOIUrl":"https://doi.org/10.1111/cen3.12824","url":null,"abstract":"<p>Inflammatory myopathy is classified into primary autoimmune myositis and secondary myositis due to various factors, such as drugs and autoimmune connective tissue diseases. Autoimmune myositis mainly consists of dermatomyositis, antisynthetase syndrome-associated myositis, immune-mediated necrotizing myopathy, and inclusion body myositis. This review aims to provide insights into muscle pathology for clinical practice and an understanding of pathophysiology in inflammatory myopathy by summarizing current knowledge about the pathology of each subform of autoimmune myositis and some secondary myositis. Dermatomyositis is associated with type I interferon upregulation. Expression of myxovirus resistance protein A (a type I interferon-induced protein) in myofibers is utilized as a sensitive diagnostic marker. Antisynthetase syndrome-associated myositis is morphologically characterized by perifascicular necrosis. A recent study suggests the presence of a characteristic immunological micromilieu suitable for plasma cells in the skeletal muscle tissue. Immune-mediated necrotizing myopathy features an active necrotic and regenerating process. In inclusion body myositis, inflammatory cellular infiltration and rimmed vacuoles reflecting autophagy disruption are observed. The lymphocytes invading myofibers are composed of a highly differentiated T-cell population, which is considered a potential therapeutic target.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"55-63"},"PeriodicalIF":0.0,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two cases illustrating different neurological aspects of HIV-escape syndrome","authors":"Merve Aktan Suzgun,&nbsp;Rümeysa Unkun,&nbsp;Osman Kizilkilic,&nbsp;Birgul Mete,&nbsp;Fehmi Tabak,&nbsp;Ugur Uygunoglu","doi":"10.1111/cen3.12825","DOIUrl":"https://doi.org/10.1111/cen3.12825","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>HIV escape syndrome is characterized by high viral load in the central nervous system despite having a low serum viral load and typically detected after the initiation of antiretroviral therapy during the course of HIV infection. The aim of this report was to reveal different aspects of the neurological involvement of HIV-escape syndrome and to define the discrete phenotypes of HIV-escape syndrome characterized by predominant inflammation or HIV-associated neurocognitive disorder.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>Two cases are presented, both were followed collaboratively by neurology and infectious diseases clinics, where the ones in which neurologic complaints associated with HIV-positivity aggravated by development of HIV-escape syndrome. The first case, investigated for progressive vision loss, represented the inflammatory course of HIV-escape with vasculitic involvement on imaging, positive serum anti-NMDA-R antibody, and good response to immunotherapy. On the other hand, the second case, who presented with progressive confusion and difficulty in walking, exemplifies the HIV-associated neurocognitive disorder with parenchymal atrophy, no evidence of inflammation, and benefit only from antiretroviral treatment modifications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>With regard to the discussions detailed herein, identifying HIV-escape syndrome as a balance of viral colonization and antiviral defense dynamics rather than a homogeneous clinical entity will broaden the clinical approaches needed. It should be particularly borne in mind that the initial neurological status may be exacerbated if HIV-escape syndrome develops.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"282-287"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can specific dietary patterns and lifestyle habits influence the progression of intracranial aneurysm lesions?","authors":"Vivig Shantha Kumar,&nbsp;Nerella Resheek,&nbsp;Vignarth Shantha Kumar,&nbsp;Ruthvik Thaghalli Sunil Kumar","doi":"10.1111/cen3.12801","DOIUrl":"https://doi.org/10.1111/cen3.12801","url":null,"abstract":"<p>The progression of intracranial aneurysm lesions involves complex mechanisms influenced by various factors, including inflammation, oxidative stress and endothelial dysfunction. This comprehensive review delves into the intricate interplay between specific dietary patterns and the progression of intracranial aneurysm lesions. Understanding the impact of these dietary factors on inflammation, oxidative stress and endothelial dysfunction offers valuable insights into noninvasive strategies for managing intracranial aneurysm progression, addressing a critical gap in current therapeutic approaches.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"265-281"},"PeriodicalIF":0.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid-related imaging abnormalities in a woman with apolipoprotein E ε4 homozygotes treated with lecanemab for Alzheimer's disease","authors":"Moeko Noguchi-Shinohara,&nbsp;Junji Komatsu,&nbsp;Kenjiro Ono","doi":"10.1111/cen3.12821","DOIUrl":"https://doi.org/10.1111/cen3.12821","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Lecanemab (Leqembi®) is an anti-amyloid monoclonal antibody used for the treatment of Alzheimer's disease (AD). However, side effects may occur with lecanemab, including amyloid-related imaging abnormalities (ARIA), especially in patients with apolipoprotein E ε4 (<i>APOE4</i>) homozygous.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 69-year-old woman had a 2-year history of worsening memory symptoms and was diagnosed with mild cognitive impairment due to AD. Because she carries two copies of the E4 allele of <i>APOE</i>, her doctor did not recommend lecanemab treatment. However, she strongly desired lecanemab treatment and received four infusions of lecanemab. She had no symptoms or neurological abnormalities, but a head MRI before the fifth infusion showed moderate radiographic ARIA; therefore, she was admitted and treated with steroids. One month later, a head MRI showed the ARIA had disappeared.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The indications of lecanemab treatment for patients with <i>APOE4</i> homozygous must be carefully considered due to the higher risk of ARIA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"254-257"},"PeriodicalIF":0.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk of progressive multifocal leukoencephalopathy in patients with multiple sclerosis treated with low-dose natalizumab following fingolimod","authors":"Masami Tanaka,&nbsp;Kazuo Nakamichi,&nbsp;Keiko Tanaka","doi":"10.1111/cen3.12820","DOIUrl":"https://doi.org/10.1111/cen3.12820","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Progressive multifocal leukoencephalopathy (PML) may rarely develop in multiple sclerosis (MS) patients treated with certain disease-modifying drugs. A female patient weighing 40 kg developed PML with 12 copies/mL of prototype JC virus (JCV) DNA in the cerebrospinal fluid after 11 y of 4 mg/kg every 6 wk with natalizumab (NTZ) and intermittent holidays of fingolimod (FTY). The aim of this study was to analyze the PML risk of this case.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The lymphocyte subsets of CD4⁺ CD62L⁺ (central memory) and CD8⁺ CD62L⁻ (effector memory) were analyzed. Additionally, the total dosage per kg for 1 y before the onset of PML and the transition of the JCV index were assessed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In PML-naïve MS patients, both lymphocyte-subset counts decreased during FTY therapy but recovered after FTY cessation. However, in this PML patient the recovery took more than 2 y. In the PML patient, the JCV index increased by 1.17 over 1 y until 10 mo before the onset of PML.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Although each factor alone is not sufficient to pose a risk in our present PML patient, the presence of multiple factors may increase the risk of PML. Administering drugs such as NTZ, which carry a PML risk, to patients with a history of FTY treatment warrants caution. Dosage and interval adjustments of NTZ should be considered. Our study suggests the possibility that FTY may increase PML risk, highlighting the importance of considering the history of immunosuppressive drug therapy when administering NTZ in MS patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"227-235"},"PeriodicalIF":0.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Performance evaluation of CXCL10 ELISA “cosmic” kit to measure CXCL10 in cerebrospinal fluid of patients with HTLV-1-associated myelopathy","authors":"Riyoko Ko,&nbsp;Katsunori Takahashi,&nbsp;Yasuo Kunitomo,&nbsp;Kenichiro Tanabe,&nbsp;Naoko Yagishita,&nbsp;Junji Yamauchi,&nbsp;Natsumi Araya,&nbsp;Makoto Nakashima,&nbsp;Erika Horibe,&nbsp;Takahiro Shimizu,&nbsp;Tomoo Sato,&nbsp;Yoshihisa Yamano","doi":"10.1111/cen3.12822","DOIUrl":"https://doi.org/10.1111/cen3.12822","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to validate the clinical utility of cerebrospinal fluid (CSF) CXCL10 measurements in HTLV-1-associated myelopathy (HAM) using a CXCL10 ELISA “Cosmic” kit, a more widely applicable method than cytometric bead array (CBA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>CSF CXCL10 levels were measured in 165 samples from 111 patients with HAM and 18 controls using a CXCL10 ELISA “Cosmic” kit. We assessed the following: (1) CSF CXCL10 concentrations by HAM activity level (high, moderate, and low) versus controls; (2) correlation with CBA; (3) cutoff values, sensitivity, and specificity for differentiating among HAM activity levels; (4) changes in HAM activity after steroid therapy; and (5) relationship between HAM activity and prognosis in patients undergoing steroid therapy. A correlation coefficient of ≥0.9 with CBA was the primary endpoint.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The median CSF CXCL10 levels in the high, moderate, low, and control groups were 4016.0, 841.0, 112.8, and 102.5 pg/mL, respectively. The ELISA findings were highly correlated with the CBA findings (<i>r</i> = 0.99). Cutoff values were set at 2500 pg/mL (sensitivity, 93.3%; specificity, 100%) to distinguish between high and moderate activity and 180 pg/mL (sensitivity, 81.8%; specificity, 100%) for low to moderate activity comparable to CBA. The new cutoffs enabled the detection of HAM activity changes and prediction of motor disability progression under steroid therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CXCL10 ELISA “Cosmic” kit findings were strongly correlated with CBA findings, meeting the primary endpoint and demonstrating comparable sensitivity and specificity for distinguishing HAM activity. This product shows a promising ability to determine the therapeutic strategy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"258-264"},"PeriodicalIF":0.0,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}