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. 2024 Sep 12;12:149. doi: 10.1186/s40478-024-01858-0

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© The Author(s) 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/.

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Fig. 3 — FP802 restores deregulated retinal gene expression in the SOD1^G93A ALS mouse model. mRNA levels of Bdnf, cFos, Npas4 and Inhibin beta A were assessed by RT q-PCR in WT, SOD1^G93A vehicle-treated, and SOD1^G93A FP802-treated mice at 20 weeks. Statistical test: one-way analysis of variance (ANOVA) with post-hoc Tukey’s multiple comparisons test. n, WT = 9; SOD1^G93A 20W (Veh) = 12; SOD1^G93A 20W (FP802) = 11. Single eyes per mouse. ∗p < 0.05, ∗∗p < 0.01