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. 2021 Apr 30;4:509. doi: 10.1038/s42003-021-02034-z

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© The Author(s) 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a–c GFAP staining in lumbar spinal cord from Wt, SOD1 + P and SOD1 + E mice at day 130 indicating increased number of reactive astrocytes in the ventral horn in SOD1 + P mice (arrows) compared to Wt and SOD1 + E mice. d–f IBA1 staining in lumbar spinal cord from Wt, SOD1 + P and SOD1 + E mice at day 130, indicating increased labeling and infiltration of reactive microglia in the ventral horn in SOD1 + P mice (arrows) compared to SOD1 + E and Wt mice. g–i ChAT staining in lumbar spinal cord from Wt, SOD1 + P and SOD1 + E mice at day 130 indicating decreased labeling in SOD1 + P mice (arrows) and pathological morphology of neurons. All images are presented with x16 magnification. N = 2–4 animals per group. WT = wild-type, SOD1 = SOD1 G93A genotype, E = etomoxir, P = placebo.