Clinical and Experimental Neuroimmunology最新文献

{"title":"Neuroinflammation and neuroimmunology in Alzheimer's disease","authors":"Koji Yamanaka","doi":"10.1111/cen3.12750","DOIUrl":"10.1111/cen3.12750","url":null,"abstract":"Neuroinflammation, mediated by activated glial cells and infiltrated lymphocytes, leads to the subsequent production of pro-inflammatory cytokines and related molecules. It is associated with the pathomechanisms of various neurodegenerative diseases, including Alzheimer's disease (AD). Microglia, innate immune cells in the central nervous system, are the principal component of neuroinflammation in health and disease. In particular, the phenotypic heterogeneity of microglia has been extensively examined through single-cell RNA sequencing technology, providing a clue to further understanding of neuroinflammation in AD and related neurological diseases. In addition, the role of brain lymphocytes has gained attention in the disease setting. In the past, the central nervous system is known to be an immuneprivileged tissue in which adaptive immunity and inflammation are highly restricted and controlled. However, an increasing number of reports show the detrimental and protective role of T lymphocytes in AD rodent models. In this issue of Clinical and Experimental Neuroimmunology, we invited three review articles by leading researchers in the fields of AD and neuroimmunology. Saito et al. reviewed the role of neuroinflammation in rodent models for AD. The authors have contributed significantly to the development of novel mouse models of AD, such as App knock-in mice. In this review, they focused on the role of the glial cell network in the AD continuum, the pathological sequence of amyloid β, tau and neurodegeneration in AD, and discussed the contribution of disease-associated microglia/homeostatic microglia in disease. Furthermore, they discussed the brain–periphery interaction in AD pathogenesis, which is a hot topic in AD research. Finally, multimorbidity in AD pathogenesis was discussed based on the clinical evidence. Chihara et al. reviewed the role of T lymphocytes in AD pathogenesis. Prominent T-lymphocyte infiltration, with its contribution to disease development and progression, is well known in multiple sclerosis. Increased permeability of the blood–brain barrier and infiltration of T lymphocytes have been documented in various studies using the human AD brain. In this regard, further investigation of the immune mechanisms resulting from T-cell infiltration into the central nervous system during disease initiation and exacerbation is required. They also provided an extensive review on the contribution of each subset of T lymphocytes in various AD models. Although the effects of each T lymphocyte on AD pathology are variable among AD mouse models, we need to carefully investigate the role of T lymphocytes in AD pathogenesis. Maekawa and Yamanaka reviewed the role of sex steroid hormone in AD, based on human and experimental evidence. As the incidence and prevalence of AD are dominant in women, the putative roles of sex hormones in AD pathology have been investigated. Although the role of estrogens was extensively investigated in the studies of ","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"78-79"},"PeriodicalIF":0.0,"publicationDate":"2023-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48658686","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 of unilateral cortical fluid-attenuated inversion recovery-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein-associated encephalitis with seizures (FLAMES)","authors":"Kunihiko Ishizawa,&nbsp;Osamu Iwasaki,&nbsp;Hironori Oka,&nbsp;Takashi Sugawara,&nbsp;Masakuni Amari,&nbsp;Takeshi Kawarabayashi,&nbsp;Koichi Okamoto,&nbsp;Kimihiko Kaneko,&nbsp;Toshiyuki Takahashi,&nbsp;Yoshio Ikeda,&nbsp;Masamitsu Takatama,&nbsp;Mikio Shoji","doi":"10.1111/cen3.12753","DOIUrl":"10.1111/cen3.12753","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a rare inflammatory disease of the central nervous system. Unilateral cortical fluid-attenuated inversion recovery-hyperintense lesions in anti-MOG-associated encephalitis with seizures (FLAMES) has recently been proposed as a subcategory of MOGAD. FLAMES is characterized by fluid-attenuated inversion recovery (FLAIR) imaging showing hyperintense cortical lesions in MOG-associated encephalitis with seizures.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>We herein report two cases of unilateral cortical FLAMES. The first case was a 29-year-old woman who developed headaches, fever, convulsions and right hemiparesis. Brain FLAIR magnetic resonance imaging (MRI) showed hyperintense cortical lesions on the left side. The second case was a 37-year-old women who developed headaches and fever. Brain FLAIR MRI showed hyperintense cortical lesions on the left side. Both cases were positive for anti-MOG antibodies in cerebrospinal fluid and serum, and were diagnosed with unilateral cortical FLAMES in MOGAD. Both patients were treated with intravenous methylprednisolone followed by oral corticosteroids, which improved MRI findings and clinical symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Both patients were diagnosed with MOGAD due to characteristic unilateral cortical encephalitis on brain FLAIR MRI. Unilateral cortical FLAMES is an important clue for the clinical diagnosis of MOGAD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"133-137"},"PeriodicalIF":0.0,"publicationDate":"2023-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44532334","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":"Post-COVID-19 vaccination Guillain–Barré syndrome with sensory ataxia, gaze-evoked nystagmus, mental-status change and positive pathological reflex","authors":"Nanami Saso,&nbsp;Shuta Toru,&nbsp;Keiichi Iwasaru,&nbsp;Hiroaki Yokote,&nbsp;Toshiki Uchihara","doi":"10.1111/cen3.12754","DOIUrl":"10.1111/cen3.12754","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Various neurological disorders have been reported after vaccination against coronavirus disease 2019, one of which is Guillain–Barré Syndrome (GBS).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>We report a case of a 73-year-old woman who developed GBS and extra-GBS manifestations 19 days after the second dose of BNT162b2 mRNA vaccine. She presented lower limb predominant muscle weakness and loss of tendon reflexes. Nerve conduction study showed acute motor and sensory axonal neuropathy. In addition, she developed notable deep sensory ataxia, and showed positive pathological reflex, gaze-evoked nystagmus and altered consciousness, which suggested brainstem involvement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first coronavirus disease 2019 vaccine-related GBS complicated with such central nervous system manifestations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"142-145"},"PeriodicalIF":0.0,"publicationDate":"2023-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41821434","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":"Neuropilin-1 (NRP1): A new marker for pathogenic autoreactive T-helper cells in autoimmune disease","authors":"Ben J. E. Raveney,&nbsp;Takashi Yamamura,&nbsp;Shinji Oki","doi":"10.1111/cen3.12751","DOIUrl":"10.1111/cen3.12751","url":null,"abstract":"Inflammation in the central nervous system (CNS) leads to local damage causing peripheral disability. Adaptive immune responses may lead the way in autoimmune neuroinflammatory disease, such as multiple sclerosis (MS), as indicated by large genome-wide association studies, histologic analysis, and the efficacy of drugs targeting lymphocytes. 1 Research from our group and others indicates a previously underappreciated key role for T-helper (Th) cells in progressive MS and other neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD). 2,3 Such Th cells initiate neuroinflammation after becoming inappropriately activated against self-antigen, leading to immune responses against self-tissues. Rapid identification of aberrant Th cells would","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"126-127"},"PeriodicalIF":0.0,"publicationDate":"2023-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46238916","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":"Bilateral longitudinally extensive optic perineuritis post-COVID-19 presenting as “idiopathic” intracranial hypertension: A case report","authors":"Mohammad Aladawi,&nbsp;Daniel Crespo,&nbsp;Renfeng Xu,&nbsp;Rana Zabad,&nbsp;Amrita-Amanda Vuppala","doi":"10.1111/cen3.12749","DOIUrl":"10.1111/cen3.12749","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Severe acute respiratory syndrome coronavirus 2 (SARSCoV2) has been associated with several neuro-ophthalmic manifestations. We report a case of bilateral longitudinally extensive optic perineuritis suspected due to SARSCoV2.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 32-year-old woman developed headaches, photophobia, pulsatile tinnitus, and blurred vision 8 d after having a positive SARS-CoV-2 qualitative polymerase chain reaction (PCR) testing for coronavirus disease 2019 (COVID-19). She was diagnosed with and treated for idiopathic intracranial hypertension (IIH) elsewhere. Repeat evaluation at our institution showed a poor visual acuity in both eyes with Frisen grade II papilledema and cotton wool spots on fundoscopic examination. Orbital magnetic resonance imaging (MRI) showed bilateral longitudinally extensive optic nerve sheath enhancement. Repeat lumbar puncture revealed an elevated cerebrospinal fluid (CSF) opening pressure and protein, a finding that is incompatible with the diagnosis of IIH. Myelin oligodendrocyte glycoprotein, aquaporin-4 (AQP4)-IgG antibodies, and other serological tests for optic neuritis were unremarkable. Her visual acuity partially improved after corticosteroids. With the growing association of demyelinating disorders and COVID-19, unremarkable serological workup, and temporal relation of the patient's symptoms to the infection, we believe that her diagnosis is SARS-CoV-2 associated bilateral optic neuritis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>There is a growing association between demyelinating disorders and COVID-19 and COVID-19 vaccination, and it is essential to recognize CSF abnormalities that are incompatible with a diagnosis of IIH, such as increased protein in our case, and may lead to an incorrect diagnosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"128-132"},"PeriodicalIF":0.0,"publicationDate":"2023-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49199311","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":"Multifocal motor neuropathy with conduction block that was shown by the flexor digitorum profundus muscle innervated from the ulnar nerve","authors":"Kazuyuki Saito,&nbsp;Hiroaki Yokote,&nbsp;Shuta Toru","doi":"10.1111/cen3.12748","DOIUrl":"10.1111/cen3.12748","url":null,"abstract":"To the Editor, Multifocal motor neuropathy (MMN) is a rare immune-mediated neuropathy characterized by progressive asymmetric limb weakness with the expression of anti-GM1 immunoglobulin M (IgM) antibodies. Conduction block (CB) shown by nerve conduction studies (NCS) is the most important feature for its diagnosis. A 28-year-old Japanese woman presented with a week-long history of progressive right hand muscle weakness without any sensory dysfunction. Her grip strength was 12/25 kg (right/left), the muscle strength of both the abductor pollicis brevis and abductor digiti minimi was 5/5. That of both the wrist extensor and wrist flexor was 5/5 according to the Medical Research Council grade. Her tendon reflexes were normal in the upper and lower limbs. The Babinski sign was bilaterally negative. Routine NCS recorded from the abductor pollicis brevis (Figure 1a) and abductor digiti minimi (Figure 1b) was in the normal range (skin temperature was maintained at 32 C). A cerebrospinal fluid examination detected no cells and showed a normal protein concentration (22.3 mg/ dL). Serum immunoglobulin G (1603 mg/dL) and IgM (166 mg/dL) were within the normal range, and serum anti-nuclear antibodies were negative. Serological testing for anti-ganglioside antibodies were positive for anti-GM1 IgM (+) and anti-GalNAc-GD1a IgM (++) antibodies. We initially suspected MMN without CB. The patient was given a 5-day course of high-dose intravenous immunoglobulin (IVIG) therapy (0.4 g/kg/day). Her right grip strength improved to 25 kg (left 25 kg). Both the anti-GM1 IgM (+) and antiGalNAc-GD1a IgM (++) antibodies were still positive 8 weeks after the first IVIG therapy. After another 6 months, her right grip strength declined to 12 kg. The muscle strength of the flexor digitorum profundus (FDP) was 4/5 (right/left), although that of the abductor pollicis brevis, abductor digiti minimi, extensor carpi radialis longus, extensor carpi ulnaris, flexor carpi radialis, extensor digitorum communis, abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, flexor pollicis longus, wrist extensor and wrist flexor was 5/5 (right/left; Medical Research Council grade). We carried out NCS of the FDP muscle innervated from the ulnar nerve (Figure 1c), CB was shown by a 19.6% reduction in compound muscle action potentials (CMAP; 5.1 to 4.1 mV) and 33.5% reduction in the CMAP area (33.1 to 22.0 mVms) between 42 and 18 mm from the medial epicondyle with normal motor conduction velocities (Figure 1d,e; 42 to 18 mm from the medial epicondyle = 68.6 m/s). These electrophysiological findings fulfilled the European Federation of Neurological Societies' electrophysiological criteria for possible motor CB in MMN; we finally diagnosed her with MMN. IVIG therapy was effective and her right grip strength improved to 28 kg. One month after the second IVIG treatment, the CB improved to 6.5% (4.6 to 4.3 mV) for the CMAP and 9.9% for CMAP area (26.3 to 23.6 mVms) at the same d","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"146-148"},"PeriodicalIF":0.0,"publicationDate":"2023-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41301271","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":"Neuroinflammation and neuroimmunology in Alzheimer's disease: The role of T-lymphocytes in Alzheimer's disease","authors":"Norio Chihara,&nbsp;Asato Tsuji,&nbsp;Riki Matsumoto","doi":"10.1111/cen3.12747","DOIUrl":"10.1111/cen3.12747","url":null,"abstract":"<p>Alzheimer's disease (AD) is the leading cause of dementia, with the number of patients with AD expected to double in the next quarter-century. Brain deposition of amyloid-β (Aβ) and tau proteins is a necessary but insufficient condition for AD pathogenesis. There is also growing evidence to suggest that chronic neuroinflammation due to excessive microglial activation and astrocyte dysfunction exacerbates the pathophysiology of AD, but the factors that disrupt these homeostatic processes remain unclear. Research into AD pathophysiology has shown interest in the changes in adaptive T-cells, which play a pivotal role in immunity. The immune alterations in the peripheral circulation and increased blood–brain-barrier permeability observed in patients with AD, even in the initial stages of the disease, require investigation of the immune mechanisms resulting from T-cell infiltration into the central nervous system (CNS) during disease initiation and exacerbation. Since T-cells play a two-faceted role in the CNS immune response, including pathogenic and neuroprotective roles, the role of T-cells in AD has been debated. Memory T-cells reside in the brain and communicate with glial cells and neurons. In this review, the role of immune responses in AD is discussed, focusing on the contribution of T-cells.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 2","pages":"92-99"},"PeriodicalIF":0.0,"publicationDate":"2023-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43294682","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":"Cotard syndrome in anti-adenylate kinase 5 autoantibodies limbic encephalitis","authors":"Aldo F. Costa,&nbsp;Alba Rodríguez","doi":"10.1111/cen3.12746","DOIUrl":"10.1111/cen3.12746","url":null,"abstract":"Cotard syndrome (CS) has been reported in patients with anti-N-methyl-D-Aspartate receptor (NMDAr) autoantibodies encephalitis, but not in limbic encephalitis (LE) associated with other autoantibodies. Clinical features of LE associated with autoantibodies against adenyl kinase 5 (AK5), a specific nucleoside monophosphate kinase of the central nervous system with crucial metabolic functions, have been previously reported in the literature. However, this is the first case reporting CS as one of the psychiatric symptoms during the clinical course. A right-handed 83-year-old woman developed memory problems, disorientation, behavioral changes and visual hallucinations in the past 2 months. Over the next 4 weeks, her symptoms progressed to a more marked deterioration of spatial orientation that interfered with daily activities and hobbies. In the following 4 weeks, she started to deny the existence of her head and occasionally she referred to herself as being dead. Neurological examination showed disorientation and anterograde amnesia. The Montreal Cognitive Assessment Scale score was 12 out of 30. Anterograde memory, attention, orientation and visuospatial/executive functions were predominately affected, whereas language and abstraction domains were spared. Routine laboratory examinations were within normal limits and infectious diseases of the central nervous system were ruled out. Cerebral spinal fluid showed lymphocytic pleocytosis (34 cells/mm, 58% lymphocytes), and hyperproteinorrachia (880 mg/L), with no presence of oligoclonal bands. Standard LE autoimmunity screening in cerebral spinal fluid was negative, including anti-NMDAR autoantibodies. A cerebral spinal fluid sample was sent to a specialized neuroimmunology laboratory for further analysis. Indirect immunofluorescence on a mouse tissue composite (TIF) showed positive anti-AK5 antibodies that were later confirmed by a cell-based assay carried out on human embryonic kidney 293 transfected cells. No other autoantibodies were positive. Brain magnetic resonance imaging showed bilateral hyperintensities in the mesial temporal lobes. The electroencephalogram and body positron emission computed tomography were unremarkable. The patient received 5-day intravenous immunoglobulin in combination with intravenous methylprednisolone (1 g/day). Over the next 3 months, the clinical course was unfavorable, and she underwent two cycles of rituximab. Cotard delusion persisted despite treatment with high doses of quetiapine. To the best of our knowledge, there are 30 reported cases of LE associated with anti-AK5 antibodies, and the present case is the first to report CS as a part of the clinical features. As in this case, patients with anti-AK5 encephalitis usually present a particularly unsatisfactory response to immunotherapy. Among the reported cases, most of the patients developed dementia due to rapidly progressive memory deficits, and approximately 50% of patients developed hippocampal atrophy. It mig","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 3","pages":"153-154"},"PeriodicalIF":0.0,"publicationDate":"2023-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42833164","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 thank you note to our reviewers","authors":"","doi":"10.1111/cen3.12741","DOIUrl":"10.1111/cen3.12741","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 1","pages":"74"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42763966","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":"The 34th Annual Meeting of the Japanese Society for Neuroimmunology (JSNI)","authors":"","doi":"10.1111/cen3.12738","DOIUrl":"https://doi.org/10.1111/cen3.12738","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"14 1","pages":"69-73"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50133855","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}