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. 2024 Feb 5;19:14. doi: 10.1186/s13024-023-00691-8

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© The Author(s) 2024, Corrected publication. February 2024

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 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. 5 — ALS model mice recapitulate features of ferroptosis and neurotoxic glia evident in human ALS-affected spinal cord. a-d Markers associated with iron are perturbed in spinal cord of transgenic SOD1^G37R ALS model mice (ALS-Tg) compared to non-transgenic littermates (Control), including elevated iron, diminished ferroxidase activity and altered expression of iron handling genes. e-h Spinal cord tissue from transgenic SOD1^G37R ALS model mice display features of ferroptosis, including elevated lipid peroxidation, diminished GPX4 protein level, and altered transcripts for ferroptosis related genes. i, j Relative expression changes for genes associated with neurotoxic glial activation in spinal cord of SOD1^G37R and control mice. Violin plots in j represent overall transcript signature for features indicated, derived from heatmap data shown in i, including genes associated with neurotoxicity in vitro (Neurotoxic; shown in Supplementary Fig. 7). k Representative immunofluorescence for microglial marker IBA1 (magenta), ferroptosis-related protein ALOX5 (green) and nuclear marker DAPI (blue) in spinal cord ventral horn of SOD1^G37R and control mice. l Microglial ALOX5 quantitated from k. m Representative immunofluorescence for IBA1 (magenta), ferroptosis-related protein LPCAT3 (green) and DAPI (blue) in spinal cord ventral horn of SOD1^G37R and control mice. n Microglial LPCAT3 quantitated from m. Data in e and f are expressed relative to controls. P values show significant differences where indicated. Data points (a, b, d-f, h, j, l, n) represent individual SOD1^G37R or control animals. Error margins in a, b, e, f, l, n are S.E.M. Values in transcript heatmaps (c, g, i) represent z-scores for individual SOD1^G37R or control animals, and crosses represent excluded samples. Violin plots in d, h, j represent overall transcript signature derived from heatmap data shown in c, g, i, respectively, where solid lines represent median, dotted lines represent 25^th/75^th percentiles, truncated at min-max values. Outline of IBA1-positive microglia are overlaid with ALOX5 and LPCAT3 in k and m, respectively. Scale bar (k, m) = 20 µm