Visual dysfunction in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis: a review

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dc.contributor.authorT Shin-
dc.contributor.authorM Ahn-
dc.contributor.authorJ Kim-
dc.contributor.authorKyungsook Jung-
dc.contributor.authorC Moon-
dc.contributor.authorM D Kim-
dc.date.accessioned2021-07-10T03:30:55Z-
dc.date.available2021-07-10T03:30:55Z-
dc.date.issued2021-
dc.identifier.issn0893-7648-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/24477-
dc.description.abstractVisual disabilities in central nervous system autoimmune diseases such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are important symptoms. Past studies have focused on neuro-inflammatory changes and demyelination in the white matter of the brain and spinal cord. In MS, neuro-inflammatory lesions have been diagnosed in the visual pathway; the lesions may perturb visual function. Similarly, neuropathological changes in the retina and optic nerves have been found in animals with chronic EAE. Although the retina and optic nerves are immunologically privileged sites via the blood-retina barrier and blood-brain barrier, respectively, inflammation can occur via other routes, such as the uvea (e.g., iris and choroid) and cerebrospinal fluid in the meninges. This review primarily addresses the direct involvement of the blood-retina barrier and the blood-brain barrier in the development of retinitis and optic neuritis in EAE models. Additional routes, including pro-inflammatory mediator-filled choroidal and subarachnoid spaces, are also discussed with respect to their roles in EAE-induced visual disability and as analogues of MS in humans.-
dc.publisherSpringer-
dc.titleVisual dysfunction in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis: a review-
dc.title.alternativeVisual dysfunction in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis: a review-
dc.typeArticle-
dc.citation.titleMolecular Neurobiology-
dc.citation.number7-
dc.citation.endPage3493-
dc.citation.startPage3484-
dc.citation.volume58-
dc.contributor.affiliatedAuthorKyungsook Jung-
dc.contributor.alternativeName신태균-
dc.contributor.alternativeName안미정-
dc.contributor.alternativeName김정태-
dc.contributor.alternativeName정경숙-
dc.contributor.alternativeName문창종-
dc.contributor.alternativeName김문두-
dc.identifier.bibliographicCitationMolecular Neurobiology, vol. 58, no. 7, pp. 3484-3493-
dc.identifier.doi10.1007/s12035-021-02355-4-
dc.subject.keywordDemyelination-
dc.subject.keywordExperimental autoimmune encephalomyelitis-
dc.subject.keywordMultiple sclerosis-
dc.subject.keywordOptic neuritis-
dc.subject.keywordRetinitis-
dc.subject.localDemyelination-
dc.subject.localexperimental autoimmune encephalomyelitis-
dc.subject.localExperimental autoimmune encephalomyelitis-
dc.subject.localMultiple sclerosis-
dc.subject.localmultiple sclerosis-
dc.subject.localOptic neuritis-
dc.subject.localRetinitis-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
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