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. 2020 Jun 6;17:175. doi: 10.1186/s12974-020-01849-7

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© The Author(s) 2020

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 — Time course of injury-induced functional, inflammatory, and neuronal changes in the SOD1 rat. This figure summarizes the longitudinal effects of mutant SOD1 protein both on motor function and cellular pathophysiology after a single sciatic nerve injury. While WT animals recovered fully from the injury within 5 weeks, they had only mild microgliosis/astrocytosis in the acute recovery stage. In contrast, injured SOD1 animals failed to recover and showed increased and sustained microgliosis followed by a premature astrocytic recruitment and neuronal synaptic loss. This model combines an environmental insult with a genetic defect that can help elucidate the functional and physiological effects of ALS disease onset and progression that could be used to develop targeted therapeutics (taken from [18] with the permission)