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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Genetic ablation of Sarm1 attenuates expression and mislocalization of phosphorylated TDP-43 after mouse repetitive traumatic brain injury

Fig. 1

Genetic ablation of Sarm1, but not Sarm1 haploinsufficiency, mitigates rTBI-associated functional deficits and mortality. (A) While all rTBI groups lost weight after rTBI, Sarm1−/− mice recovered their weight faster than Sarm1+/+ and Sarm1+/−mice (p = 0.003 for group effects, p < 0.001 for time effects, p < 0.001 for group x time interaction). (B) While neurological deficits were significantly attenuated in both Sarm1−/− and mice Sarm1+/− up to 1 week post rTBI, only Sarm1−/− mice showed persistent protection up to the 4-week time point (p = 0.003 for group effects, p < 0.001 for time effects, p < 0.001 for group x time interaction). (C) Successive rTBI prolonged the time of the return of the righting reflex without difference between groups (group effect p = 0.219, time effect p = 0.016, group x time p = 0.600; *p < 0.05 versus TBI 1 [ref.]). (D) Sarm1−/− mice had a significantly lower seizure burden when compared to wild type mice (ANOVA on Ranks with post-hoc Tukey test). (E) Genetic ablation of Sarm1 significantly reduced rTBI-associated mortality. Numbers in parenthesis indicate the number of mice that died per the total number of mice in each group. Data in bar graphs are mean ± sem. *p < 0.05, **p < 0.01, ***p < 0.001

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