Clinical and Experimental Neuroimmunology最新文献

{"title":"Multifactorial glial responses and their contributions to Alzheimer's disease continuum","authors":"Masanori Hijioka,&nbsp;Tatsuya Manabe,&nbsp;Takashi Saito","doi":"10.1111/cen3.12745","DOIUrl":"10.1111/cen3.12745","url":null,"abstract":"<p>Alzheimer's disease (AD) is the most common neurocognitive disorder. Various factors are intricately intertwined before clinical symptoms appear, although both amyloid-β peptide deposition and neurofibrillary tangle formation (i.e. pathological hallmarks of the AD brain) are established. Among such factors, glial responses have been increasingly recognized as important roles in the progression of these pathologies and viewed as one component of the AD continuum. However, the detailed molecular and cellular mechanisms of glial function underlying AD pathogenesis remain to be elucidated. Recent studies showed that peripheral immunity, gut microbiota or environmental factors influence brain pathophysiologies through communication with glial cells in the brain. This disease complexity makes understanding AD etiology difficult and hinders the development of effective therapeutic strategies to tackle this disease. Conversely, aged patients often suffer from multiple – not a single – diseases as multimorbidity, and AD pathogenesis might be related to pathologies caused by other diseases. Hence, investigating AD as a systemic disease has become critical for identifying therapeutic interventions. This review aimed to summarize current knowledge on AD research and share perspectives for understanding glial functions regarding AD pathophysiology.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"82-91"},"PeriodicalIF":0.0,"publicationDate":"2023-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41548013","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":"Identification of neuromuscular medullary thymic epithelial cells in thymoma with myasthenia gravis","authors":"Tatsusada Okuno,&nbsp;Yoshiaki Yasumizu,&nbsp;Hideki Mochizuki","doi":"10.1111/cen3.12743","DOIUrl":"https://doi.org/10.1111/cen3.12743","url":null,"abstract":"Autoimmune diseases lead to antibodies mistakenly recognizing and attacking host cells as foreign invaders. One such disease is myasthenia gravis (MG), where the antibodies target neuromuscular-associated proteins, including the acetylcholine receptor. MG commonly occurs in patients with thymoma; however, the reasons for this remain unclear. Recently, a bioinformatic approach was undertaken to examine the relationship between these two diseases.","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"80-81"},"PeriodicalIF":0.0,"publicationDate":"2023-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50125589","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":"Transverse myelitis following bivalent COVID-19 booster vaccine and quadrivalent seasonal influenza vaccine","authors":"Teresa L. Xiao,&nbsp;Alexandre Zaharia,&nbsp;Anas S. Al-Smadi,&nbsp;Caleb J. Murphy","doi":"10.1111/cen3.12742","DOIUrl":"10.1111/cen3.12742","url":null,"abstract":"<p>We present a case of acute partial transverse myelitis (TM) that developed 6 d following covaccination with a bivalent COVID-19 booster vaccine and quadrivalent influenza vaccine. Although initial imaging of the thoracic spine was nonspecific, repeat magnetic resonance imaging (MRI) showed a T2 hyperintense lesion with contrast enhancement, consistent with TM. The risk of rare but catastrophic neurologic complications following the bivalent COVID-19 booster vaccine and/or covaccination with COVID-19 and influenza vaccines is the subject of ongoing investigation in the medical community.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"138-141"},"PeriodicalIF":0.0,"publicationDate":"2023-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12742","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48020342","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":"The Japanese clinical guidelines 2022 for myasthenia gravis and Lambert–Eaton myasthenic syndrome","authors":"Hiroyuki Murai,&nbsp;Kimiaki Utsugisawa,&nbsp;Masakatsu Motomura,&nbsp;Tomihiro Imai,&nbsp;Akiyuki Uzawa,&nbsp;Shigeaki Suzuki","doi":"10.1111/cen3.12739","DOIUrl":"10.1111/cen3.12739","url":null,"abstract":"<p>The revised Japanese clinical guidelines for myasthenia gravis (MG) and Lambert–Eaton myasthenic syndrome (LEMS) were published in 2022. The notable points in these guidelines (GLs) are as follows: (i) these are the first Japanese GLs to include a description of LEMS; (ii) diagnostic criteria of MG are revised to lessen the incidence of false negative patients; (iii) MG is divided into six clinical subtypes; (iv) a high-dose oral steroid regimen with escalation and de-escalation schedule is not recommended by the GLs; (v) the GLs promote the early fast-acting treatment strategy initially proposed in the previous GLs; (vi) refractory MG is defined; (vii) the use of molecular targeted drugs is included; (viii) diagnostic criteria of LEMS are proposed; and (ix) treatment algorithms for both MG and LEMS are presented. These new GLs are expected to improve the patients' quality of life and will serve to bridge the present era with the molecular targeted treatment eras.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 1","pages":"19-27"},"PeriodicalIF":0.0,"publicationDate":"2023-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12739","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42857810","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":"All differential diagnoses of cerebellar ataxia should be ruled out before SARS-CoV-2 is blamed as the cause","authors":"Josef Finsterer","doi":"10.1111/cen3.12737","DOIUrl":"10.1111/cen3.12737","url":null,"abstract":"We read","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"122"},"PeriodicalIF":0.0,"publicationDate":"2022-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9877961/pdf/CEN3-9999-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10592109","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":"Epidemiological study of myasthenia gravis in Japan","authors":"Hiroaki Yoshikawa","doi":"10.1111/cen3.12736","DOIUrl":"10.1111/cen3.12736","url":null,"abstract":"<p>Myasthenia gravis (MG) is an autoimmune-mediated neurological disorder. The relationship between MG and thymic abnormalities is well recognized, and thymectomy is one of the therapies for anti-acetylcholine receptor antibody-positive MG. The major pathogenic factor is anti-acetylcholine receptor antibody followed by anti-muscle-specific kinase antibody, and commercial kits are available to detect these antibodies. Several decades ago, the prognosis of MG was not favorable; therefore, the Ministry of Health and Welfare (predecessor of the Ministry of Health, Labor and Welfare) organized a Taskforce for Intractable Diseases, which included MG, in 1972. The Taskforce carried out consecutive epidemiological studies for MG in 1973, 1987, 2006 and 2018. The four studies found: (i) increasing prevalence; (ii) increasing late- and elderly-onset; (iii) decreasing female dominancy; (iv) decreasing infantile-onset (onset age of 0–4 years); and (v) decreasing frequencies of crisis. The latest epidemiological study in Japan and studies from other countries suggest an increasing number of patients with anti-acetylcholine receptor antibody-positive MG without thymoma in the elderly. It is important to find out the causes of this phenomenon, which will improve the prevention of MG.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 1","pages":"13-18"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49494184","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":"Issue Information","authors":"","doi":"10.1111/odi.14414","DOIUrl":"https://doi.org/10.1111/odi.14414","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49037533","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":"Autoantibodies against contactin-associated protein 1 and complexes of paranode-specific proteins in chronic inflammatory demyelinating polyradiculoneuropathy","authors":"Michiaki Koga,&nbsp;Toshihiko Maeda,&nbsp;Fumitaka Shimizu,&nbsp;Takashi Kanda","doi":"10.1111/cen3.12735","DOIUrl":"10.1111/cen3.12735","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To investigate the frequency of serum autoantibodies targeting contactin-associated protein 1 (Caspr1) and its complexes with other paranode antigens, contactin-1 (CNTN1) and neurofascin 155 (NF155), in Japanese patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Sera from 26 CIDP patients, 35 patients with Guillain–Barré syndrome, and 31 healthy individuals participated. Paranodal immunoglobulin G antibodies were quantified using enzyme-linked immunosorbent assays with commercially available recombinant proteins as antigens.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Anti-Caspr1 antibodies were present in one participant (case 1, 3.8%) of CIDP, and negative in all Guillain–Barré syndrome patients and healthy participant. Case 1 was a man who developed subacute distal limb-predominant muscle weakness and sensory ataxia with postural hand tremor at 69 years-of-age, and therapeutic benefit of intravenous immunoglobulin and oral steroids was inadequate. The detected anti-Caspr1 antibodies predominantly belonged to the immunoglobulin G4 subclass, and the addition of CNTN1 to Caspr1 as an antigen increased antibody reactivity, although the increase was just 20–30% at most. The presence of autoantibodies against paranode protein complexes, including Caspr1/CNTN1, Caspr1/NF155 and Caspr1/CNTN1/NF155, was confirmed in several CIDP patients, although they also had anti-Caspr1 or anti-NF155 antibodies; thus, in our cohort, there were no patients with autoantibodies that specifically recognized paranode protein complexes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first confirmed Japanese case of anti-Caspr1 antibody-positive CIDP with a clinical signature similar to that of patients of Western origin. Our preliminary study did not identify the presence of specific antibodies against the paranode protein complexes, and the primary target antigen is likely Caspr1.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"116-121"},"PeriodicalIF":0.0,"publicationDate":"2022-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45050723","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":"A case of natalizumab-associated progressive multifocal leukoencephalopathy followed by immune reconstitution inflammatory syndrome with difficulty in the timing of immunotherapy","authors":"Takamichi Sugimoto,&nbsp;Shuichiro Neshige,&nbsp;Shiro Aoki,&nbsp;Kazuhide Ochi,&nbsp;Ruoyi Ishikawa,&nbsp;Megumi Nonaka,&nbsp;Masahiro Nakamori,&nbsp;Tomohisa Nezu,&nbsp;Kazuo Nakamichi,&nbsp;Yu Yamazaki,&nbsp;Hirofumi Maruyama","doi":"10.1111/cen3.12734","DOIUrl":"10.1111/cen3.12734","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Details regarding the clinical course of natalizumab-associated progressive multifocal leukoencephalopathy (NAT-PML) have not been reported in Japanese patients. We experienced a Japanese NAT-PML case and report it for the purpose of clarifying the challenge it posed in medical treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>Herein, we describe a 58-y-old multiple sclerosis patient who had NAT-PML with immune reconstitution inflammatory syndrome (IRIS). Before NAT-PML developed, the patient's Expanded Disability Status Scale (EDSS) score was 5.5. She received natalizumab (300 mg) every 3–7 w, and her EDSS score had not changed for 9.1 y. The John Cunningham virus (JCV) index was 0.43 before NAT-PML developed. She developed a gait disturbance when NAT-PML emerged. Natalizumab was administered a total of 108 times. The patient was diagnosed with probable NAT-PML on the basis of punctate lesions on T2-weighted imaging and a JCV-PCR result of 29 copies/ml from cerebrospinal fluid (CSF) testing. Intravenous methylprednisolone (IVMP) was initiated when the contrast-enhanced lesion was first detected, but the NAT-PML lesion was rather enlarged despite the temporary disappearance of the contrast-enhanced lesion. An obvious increase in the IgG index and a slight increase in the CSF cell count were recognized at the time the immunological response was activated. Three cycles of a 3-d course of IVMP were administered every 2 w for IRIS, and the patient's worst EDSS score was 9.5.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Treatment sequencing should be executed before the onset of NAT-PML. Changes in CSF cell count and IgG index may be useful for treatment decision; further research is needed.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"110-115"},"PeriodicalIF":0.0,"publicationDate":"2022-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48754605","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":"Level of CSF CXCL10 is highly elevated and decreased after steroid therapy in patients with autoimmune glial fibrillary acidic protein astrocytopathy","authors":"Takayuki Kikuchi,&nbsp;Naoki Takao,&nbsp;Tomoo Sato,&nbsp;Kenji Isahaya,&nbsp;Sakae Hino,&nbsp;Mayumi Kaburagi,&nbsp;Keiji Tachikawa,&nbsp;Riyoko Ko,&nbsp;Soichiro Shibata,&nbsp;Kei Kaburagi,&nbsp;Naoki Iijima,&nbsp;Heisuke Mizukami,&nbsp;Kenzo Sakurai,&nbsp;Junji Yamauchi,&nbsp;Akio Kimura,&nbsp;Takayoshi Shimohata,&nbsp;Yoshihisa Yamano","doi":"10.1111/cen3.12732","DOIUrl":"10.1111/cen3.12732","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To examine the chemokine profile in the cerebrospinal fluid (CSF) of patients with glial fibrillary acidic protein astrocytopathy (GFAP-A), central nervous system immune-related adverse event (CNS-irAE), neurosarcoidosis (NS), neuromyelitis optica spectrum disorders (NMOSD), multiple sclerosis (MS), and human T-cell leukemia virus-1 (HTLV-1)-associated myelopathy (HAM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study included 38 patients presenting to St. Marianna University Hospital between May 2013 and November 2021 with GFAP-A, CNS-irAE, NMOSD, MS, NS, HAM and noninflammatory neurological diseases (NIND). We recorded the age, sex, duration of disease, brain/spinal lesions on magnetic resonance imaging (MRI), blood data, and measured chemokines (CXCL9, −10, −13, CCL3, −4, −17, −20, −22) in CSF. In patients with GFAP-A, clinical symptoms, and CSF CXCL10 levels were compared before and after steroid treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Patients with GFAP-A had higher CSF levels of CXCL10, CXCL13, and CCL22 (10736.1 [8786.7–149079.0] pg/ml (<i>p</i> &lt; .05), 378.4 [239.9–412.2] pg/ml (<i>p</i> &lt; .01) and 159.9 [130.5–413.9] pg/ml (<i>p</i> &lt; .01), respectively). The CSF levels of CXCL10 improved from 10736.1 [8786.7–149079.0] pg/ml to 1879.0 [783.9–4360.0] pg/ml in patients with GFAP-A by steroid therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CSF CXCL10 levels were particularly high in GFAP-A, and changes in levels after treatment correlated with clinical improvements, suggesting CXCL10 involvement in GFAP-A pathogenesis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 1","pages":"61-68"},"PeriodicalIF":0.0,"publicationDate":"2022-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48892579","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}