Figure 7.
The Swl Dync1h1 mutation does not delay disease progression in SOD1G93A mice. A, C, E, Swl/+ × SOD1G93A hemizygote; B, D, F, Loa/+ × SOD1G93A hemizygote. The Kaplan–Meier survival analysis demonstrates that Swl/SOD1G93A mice have a comparable average survival time with that of SOD1G93A/+ mice (A), whereas the average survival time of Loa/SOD1G93A mice is significantly delayed compared with that of SOD1G93A/+ mice (B; p < 0.01, log-rank test for equality of survival curves). In contrast to Swl/SOD1G93A mice (C), the body weight loss of Loa/SOD1G93A mice is significantly delayed compared with that of SOD1G93A/+ mice during the observation period (D; p < 0.01, Student's t test). Similarly, the motor function determined by forelimb grip strength test shows no significant difference between Swl/SOD1G93A mice and SOD1G93A/+ mice (E), whereas Loa/SOD1G93A mice have a significant delay in motor dysfunction compared with that of SOD1G93A/+ mice during the observation period (F; p < 0.01, Student's t test).