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. 2017 Jul 12;7:5235. doi: 10.1038/s41598-017-05313-0

Figure 2.

Figure 2

Pharmacological inhibition of GCase activity delays disease onset and improves motor functions in SOD1G86R mice. (A) Body mass evolution in wild type mice after 10 days of CBE treatment (n = 5/group). (B) Muscle strength of wild type mice after 10 days of CBE treatment (n = 5/group). (C) Total β-glucocerebrosidase activity measured in the spinal cord lysate of wild type mice (n = 5). (D,E) GlcCer (D) and gangliosides (E) levels in the spinal cord of wild type mice after CBE treatment (n = 5/group). (F) Body mass evolution in SOD1 and WT mice (n = 7 for WT groups, n = 12 for SOD1 veh and n = 14 for SOD1 CBE). (G) Kaplan-Meier showing time to onset of muscle strength loss in SOD1G86R mice (n = 12 for SOD1 veh and n = 14 for SOD1 CBE, p < 0.02). (H–L) Catwalk analysis showing representative pattern of strides of symptomatic SOD1G86R mice (H), and average speed (I), stride length (J), paw swing (K) and stand index (L) in 95 days old mice. Mean ± SEM, *p < 0.05.