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. 2007 Mar 26;104(14):6072–6077. doi: 10.1073/pnas.0610923104

Fig. 2.

Fig. 2.

CCS overexpression accelerates G93A-SOD1-induced disease. (A) Mass (gms) comparison of line 17 CCS/G93A-SOD1 dual mice with controls. By day 6, CCS/G93A-SOD1 dual mice weigh significantly less (∗, P = 0.016), whereas there is no difference in mass among NTG, CCS, and G93A-SOD1 (P = 0.377) by ANOVA (n = 7–12 for each group; values ± SEM). (B) Stride length measurements in line 17 CCS/G93A-SOD1 dual mice and controls. By day 22, CCS/G93A-SOD1 dual mice have a significantly shorter stride length (∗, P = 0.025), whereas there is no difference in stride length among controls (P = 0.685) by ANOVA (n = 7–10 for each group; values ± SEM). (C) Forepaw grip strength measurements in decigrams of line 17 CCS/G93A-SOD1 dual mice and controls. At day 26, CCS/G93A-SOD1 dual mice have significantly weaker grips (∗, P = 0.003), whereas there is no difference in grip strength among controls (P = 0.165) by ANOVA (n = 4–7 for each group; values ± SEM). (D) Kaplan–Meier survival curves from CCS (n = 15), G93A-SOD1 (n = 14), and CCS/G93A-SOD1 (n = 17) dual mice of line 17. CCS/G93A-SOD1 dual mice have significantly shortened survival (P = 0.001).