{"title":"Characterization of pathological stages in a mouse model of progressive multiple sclerosis","authors":"Satoshi Hamano , Toshiki Yoshimizu , Mutsuki Mori , Akio Iida , Toshihide Yamashita","doi":"10.1016/j.neures.2024.01.009","DOIUrl":null,"url":null,"abstract":"<div><p>The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. Pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stage in the lesion. The NOD-EAE mice showed a biphasic pattern of disease progression once in remission. The longitudinal profile of demyelination and inflammatory cell infiltration in the spinal cord was consistent with the pathological score. In the chronic phase of the disease, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. Here we describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase. This model may be useful for evaluating the efficacy of therapeutic agents and for mechanistic analysis.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"204 ","pages":"Pages 46-57"},"PeriodicalIF":2.4000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010224000233/pdfft?md5=a57978a2bd0a6a011a8ad8cd6222f835&pid=1-s2.0-S0168010224000233-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0168010224000233","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. Pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stage in the lesion. The NOD-EAE mice showed a biphasic pattern of disease progression once in remission. The longitudinal profile of demyelination and inflammatory cell infiltration in the spinal cord was consistent with the pathological score. In the chronic phase of the disease, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. Here we describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase. This model may be useful for evaluating the efficacy of therapeutic agents and for mechanistic analysis.
期刊介绍:
The international journal publishing original full-length research articles, short communications, technical notes, and reviews on all aspects of neuroscience
Neuroscience Research is an international journal for high quality articles in all branches of neuroscience, from the molecular to the behavioral levels. The journal is published in collaboration with the Japan Neuroscience Society and is open to all contributors in the world.