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Figure 4 | Acta Neuropathologica Communications

Figure 4

From: Systemic delivery of P42 peptide: a new weapon to fight Huntington’s disease

Figure 4

Aonys® NP42T treatment ameliorates behavioural deficits in R6/2 mice. (A) R6/2 mice present a foot-clasping behaviour (A’) absent in WT littermates (A). (B). Only groups treated with NP42T show a clear inhibition of clasping duration at 11wks: Two way ANOVA (F(Genotype x Treatment)1,25 = 6.4, p = 0.0179). Post-hoc comparison (Bonferroni’s test): **p < 0.01 WT (NP) vs R6/2 (NP); **p < 0.01 R6/2 (NP) vs R6/2 (NP42T), with two way ANOVA (F(Group x Time)6,78 = 1.0, p = 0.4022) similar over time. (C) Rotarod performances of wild-type (WT) or R6/2 mice treated with NP42T or with empty NP (placebo) at 6, 8 and 10 weeks of age. Motor deficit is identified in R6/2 mice already at week6. Beneficial effect is observed for R6/2 treated with NP42T: Two way ANOVA (F(group x time)6,78 = 2.362, p < 0.05) indicates that rotarod deficit of the four groups of mice was different over time. Post-hoc comparison (Bonferroni’s test): 6wks *p < 0.05 R6/2 (NP) vs R6/2 (NP42T); *p < 0.05; 8wks ***p < 0.001 WT (NP) vs R6/2 (NP); *p < 0.05 R6/2 (NP) vs R6/2 (NP42T); 10wks ***p < 0.001 WT (NP) vs R6/2 (NP); ns R6/2 (NP) vs R6/2 (NP42T). (D) Body weight of R6/2 mice is recovered by both early and late administrations of NP42T. Body weight variations were measured in WT and R6/2 mice, treated with empty NP (placebo) or with NP42T. Graphs represent the body weight evolution from 8wks to 11wks in percentage. In HD mice, NP42T inverts the curves and restores a gain of weight in pre-symptomatic. One way ANOVA: (F(3,24) = 5.2, p < 0.01). Post-hoc comparison (Fisher’s LSD): **p < 0.01 WT (NP) vs R6/2 (NP); **p < 0.01 R6/2 (NP) vs R6/2 (NP42T). Data represent means +/−SEM (n = 5-9 per group).

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