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. 2022 Nov 19;19:277. doi: 10.1186/s12974-022-02635-3

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Individualized fingolimod treatment accelerates disease recovery and decrease the histopathological damage in EAE mice. A Individualized fingolimod treatment from disease onset significantly reduced the clinical course and severity of EAE in mice (EAE-Veh N = 19; EAE-FTY720 N = 18). B, C Panoramic images of the spinal cord of one EAE-Veh (B) and one EAE-FTY720 (C) mouse stained with EC (myelin, blue). Dashed lines define the demyelinated area. D, E Detailed view of SMI-32 staining (axonal damage, red) in infiltrated areas (delimitated by dashed lines) of the spinal cord of EAE-Veh (D) and EAE-FTY720 (E) mice (nuclei are stained with Hoechst). F, G Quantification of the relative demyelination within the white matter or the axonal damage within the infiltrated area in the histological sub-cohort of EAE mice (EAE-Veh N = 9, EAE-FTY720 N = 9). Scale bar: B, C = 250 µm; D, E = 50 µm