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Hilton Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000910","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01NS105741"],"award-info":[{"award-number":["R01NS105741"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Neuroinflammation"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n              <jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>Retinal optical coherence tomography (OCT) is a clinical and research tool in multiple sclerosis, where it has shown significant retinal nerve fiber (RNFL) and ganglion cell (RGC) layer thinning, while postmortem studies have reported RGC loss. Although retinal pathology in experimental autoimmune encephalomyelitis (EAE) has been described, comparative OCT studies among EAE models are scarce. Furthermore, the best practices for the implementation of OCT in the EAE lab, especially with afoveate animals like rodents, remain undefined. We aimed to describe the dynamics of retinal injury in different mouse EAE models and outline the optimal experimental conditions, scan protocols, and analysis methods, comparing these to histology to confirm the pathological underpinnings.<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Using spectral-domain OCT, we analyzed the test-retest and the inter-rater reliability of volume, peripapillary, and combined horizontal and vertical line scans. We then monitored the thickness of the retinal layers in different EAE models: in wild-type (WT) C57Bl\/6J mice immunized with myelin oligodendrocyte glycoprotein peptide (MOG<jats:sub>35\u201355<\/jats:sub>) or with bovine myelin basic protein (MBP), in TCR<jats:sup>2D2<\/jats:sup> mice immunized with MOG<jats:sub>35\u201355<\/jats:sub>, and in SJL\/J mice immunized with myelin proteolipid lipoprotein (PLP<jats:sub>139\u2013151<\/jats:sub>). Strain-matched control mice were sham-immunized. RGC density was counted on retinal flatmounts at the end of each experiment.<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Volume scans centered on the optic disc showed the best reliability. Retinal changes during EAE were localized in the inner retinal layers (IRLs, the combination of the RNFL and the ganglion cell plus the inner plexiform layers). In WT, MOG<jats:sub>35\u201355<\/jats:sub> EAE, progressive thinning of IRL started rapidly after EAE onset, with 1\/3 of total loss occurring during the initial 2\u2009months. IRL thinning was associated with the degree of RGC loss and the severity of EAE. Sham-immunized SJL\/J mice showed progressive IRL atrophy, which was accentuated in PLP-immunized mice. MOG<jats:sub>35\u201355<\/jats:sub>-immunized TCR<jats:sup>2D2<\/jats:sup> mice showed severe EAE and retinal thinning. MBP immunization led to very mild disease without significant retinopathy.<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Retinal neuroaxonal damage develops quickly during EAE. Changes in retinal thickness mirror neuronal loss and clinical severity. Monitoring of the IRL thickness after immunization against MOG<jats:sub>35\u201355<\/jats:sub> in C57Bl\/6J mice seems the most convenient model to study retinal neurodegeneration in EAE.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12974-019-1583-4","type":"journal-article","created":{"date-parts":[[2019,11,4]],"date-time":"2019-11-04T10:02:59Z","timestamp":1572861779000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Monitoring retinal changes with optical coherence tomography predicts neuronal loss in experimental autoimmune encephalomyelitis"],"prefix":"10.1186","volume":"16","author":[{"given":"Andr\u00e9s","family":"Cruz-Herranz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Dietrich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander M.","family":"Hilla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao H.","family":"Yiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc H.","family":"Levin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Hecker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Issberner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelika","family":"Hallenberger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Cordano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus","family":"Lehmann-Horn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisanne J.","family":"Balk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Orhan","family":"Aktas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Ingwersen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charlotte","family":"von Gall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Peter","family":"Hartung","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott S.","family":"Zamvil","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dietmar","family":"Fischer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7987-658X","authenticated-orcid":false,"given":"Philipp","family":"Albrecht","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ari J.","family":"Green","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,11,4]]},"reference":[{"issue":"12","key":"1583_CR1","doi-asserted-by":"publisher","first-page":"1273","DOI":"10.1056\/NEJMcp053247","volume":"354","author":"LJ Balcer","year":"2006","unstructured":"Balcer LJ. 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Unrelated to the work presented, the authors declare the following financial disclosures: Michael Dietrich received speaker honoraria from Novartis. Hans-Peter Hartung has received fees for serving on steering committees from Biogen Idec, GeNeuro, Sanofi Genzyme, Merck, Novartis Pharmaceuticals, Octapharma, Opexa Therapeutics, Teva Pharmaceuticals, MedImmune, Bayer HealthCare, Forward Pharma, and Roche; fees for serving on advisory boards from Biogen Idec, Sanofi Genzyme, Merck, Novartis Pharmaceuticals, Octapharma, Opexa Therapeutics, Teva Pharmaceuticals, and Roche; and lecture fees from Biogen Idec, Sanofi Genzyme, Merck, Novartis Pharmaceuticals, Octapharma, Opexa Therapeutics, Teva Pharmaceuticals, MedImmune, and Roche. Klaus Lehmann-Horn received speaker honoraria and travel support from Novartis, Hoffmann-La Roche, and Merck Serono. He receives research support from Novartis. Philipp Albrecht received compensation for serving on Scientific Advisory Boards for Ipsen, Novartis, Biogen; he received speaker honoraria and travel support from Novartis, Teva, Biogen, Merz Pharmaceuticals, Ipsen, Allergan, Bayer Healthcare, Esai, UCB, and Glaxo Smith Kline; he received research support from Novartis, Biogen, Teva, Merz Pharmaceuticals, Ipsen, and Roche. Ari J. Green served on the scientific advisory board of MedImmune, Novartis, OCTIMS, Inception 5 Biosciences, and Bionure; is an associate editor of JAMA Neurology; was an editorial board member of Neurology; holds a patent for remyelination molecules and pathways; consulted for Inception 5 Sciences; received research support from Novartis Pharma OCTIMs, Inception Sciences SRA, NINDS, NIA, National MS Society, Sherak Foundation, and Hilton Foundation; holds stock or stock options in Inception 5; and served as an expert witness at Mylan v Teva Pharma. The other authors report no disclosures.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"203"}}