Fig. 2

EAE severity is enhanced in f-ATXN1^146Q/2Q and Atxn1^2Q/− mice. (A) Mean EAE clinical scores showed an identical more severe disease course in f-ATXN1^146Q/2Q and Atxn1^2Q/− mice compared to WT control mice. (B) Peak EAE clinical score for individual mice. (C) The mean aggregate EAE clinical score was higher in f-ATXN1^146Q/2Q and Atxn1^2Q/− mice compared to WT control mice. (D) Mean EAE clinical scores PID-16 and PID-30 for WT (N = 21), f-ATXN1^146Q/2Q (N = 13), and Atxn1^2Q/− mice (N = 10). Error bars represent SEM. Differences between scores on each day were assessed by two-way ANOVA with Tukey’s multiple comparison test (A, D) and one-way ANOVA with Tukey’s multiple comparison test (B, C). *(knock-in vs. wildtype; heterozygous vs. wildtype); *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001, ns, not significant