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. 2021 Mar 13;26(6):1590. doi: 10.3390/molecules26061590

Figure 1.

Figure 1

RD2RD2 treatment prevented further significant progression of motor phenotype in SOD1*G93A mice. Changes in absolute body weight (g) over time during treatment revealed significant differences between transgenic and non-transgenic mice (a). Analysis of the SHIRPA test battery to evaluate the phenotypic development of RD2RD2- and placebo-treated SOD1*G93A mice resulted in halt of phenotype progression upon treatment (b). Subdivision of the SHIRPA parameters into a motor score revealed significant inhibition of motor symptom progression in RD2RD2- vs. placebo-treated SOD1*G93A (c). Pole test analysis (d) resulted in significant conservation of motor skills in RD2RD2-treated mice, whereas the motor deficits progressed further in placebo-treated mice. All non-transgenic mice exhibited normal motor function throughout the experimental period. Data is presented as mean ± SEM. Statistical calculations were conducted by two-way RM ANOVA with Fisher’s LSD post hoc analysis, non-transgenic mice (ntg) n = 13, RD2RD2 n = 12 and placebo n = 10 for each test. Lozenges and asterisks (*) indicate a significance between treatment groups (ntg vs. RD2RD2 or ntg vs. placebo: ## p < 0.01, ### p < 0.001 and RD2RD2 vs. placebo: * p = 0.05, ** p < 0.01, *** p < 0.001).