Fig. 3

Spermidine treatment did not improve the motor impairment of CMVMJD135 mice developed motor impairment. (A) A schematic diagram illustrates that CMVMJD135 mice were treated with spermidine (3 mM) within their drinking water from 5 to 25 weeks old. Behavioural testing was conducted throughout the study and a subset of animals were euthanised at 18 weeks old and another at 25 weeks old. (B) Comparison of water intake between mice treated with spermidine and water found no significant difference (p = 0.809). (C) MJD mice had lower body weights than wild-type mice from 9 weeks old onwards (p < 0.0236), and although spermidine treatment appeared to cause decreased weights in the wild type mice, this was not a statistically significant effect. (D) Whilst mutant CMVMJD135 mice developed increased neurological scores, indicative of neurological impairment, from around 9 weeks old onwards (*p < 0.0193), treatment with spermidine did not improve this impairment (it worsened it at 7 and 12 weeks old (p < 0.0402). (E) MJD mice had decreased latencies on the rotarod compared to wild-type mice from around 9 weeks old (**p < 0.0001). Treatment with spermidine did not increase the latency before falling from an accelerating rotarod. In fact, treatment with spermidine treatment decreased the latency to fall in wild type mice compared to water treated wild type mice at 6 and 7 weeks old (***p < 0.0331). (F) MJD mice took longer to cross the balance beam than wild-type mice at 16 and 18 weeks old (**p < 0.0106). Spermidine treatment did not affect the time taken by mice to cross a balance beam, regardless of genotype. A repeated one-way ANOVA was utilised for statistical analysis followed by Tukey post hoc. Data represents mean ± SEM. Biorender.com was used to make the image in panel A