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. 2022 May 18;32(6):e13078. doi: 10.1111/bpa.13078

FIGURE 2.

FIGURE 2

mfSOD1 expression, MN phenotypes, and MN death in SOD1G93A mice. (A, B) quantification of mfSOD1 in the MN somata (A) in WT and in the three defined mfSOD1 phenotypes in SOD1G93A mice; (B) the same quantification was performed within ventral horn neuropil in relation to the age‐related disease progression (C) quantification of the abundance of the three mfSOD1 MN phenotypes in the ventral horn from WT and in SOD1G93A at distinct stages of ALS progression (ES = end‐stage). (D, E) evaluation of the numbers of healthy (D) and degenerating (E) MNs in Nissl‐stained spinal cord sections of WT and ALS at distinct ages of progression in SOD1G93A mice. Data in the graph are shown as the mean ± SEM from either 307 MNs or from 17 sections of ventral horn neuropil (n = 3 animals per group) in (A and B). (C) Total MNs from 15 to 18 spinal cord sections (n = 3 animals per group) were evaluated. ***p < 0.001; ****p < 0.0001; #p<0.05; ##p<0.005; ###p< 0.001; ####p<0.0001 (# refered to WT), one‐way analysis of variance (ANOVA), Bonferroni's post hoc test.