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. Author manuscript; available in PMC: 2016 Apr 20.
Published in final edited form as: Nat Neurosci. 2015 Dec 14;19(1):65–74. doi: 10.1038/nn.4193

Figure 1.

Figure 1

DTA mice develop a severe late-onset clinical phenotype. (a) Tamoxifen-treated Plp1-CreERT;ROSA26-eGFP-DTA mice displayed significantly reduced latency on the rotarod starting around 38 weeks after injection as compared to the control littermate (ROSA26-eGFP-DTA) mice. Control mice: 19–32 weeks, n = 5; 33 and 46–51 weeks, n = 9; 34, 35 and 43–45 weeks, n = 11; 36, 41 and 42 weeks, n = 14; 37–40 weeks, n = 15; 52 weeks, n = 7. DTA mice: 19–32 weeks, n = 4; 33 and 42 weeks, n = 10; 34 weeks, n = 12; 35 and 41 weeks, n = 11; 36–39 weeks, n = 15; 40 weeks, n = 14; 43 weeks, n = 9; 44 weeks, n = 7; 45–50 weeks, n = 5; 51–52 weeks, n = 3. Significance between control and DTA mice: 38 weeks, P = 0.0005; 39 weeks, P = 0.0094; 40 weeks, P = 0.0024; 41 weeks, P = 0.0002; 42 weeks, P = 0.0025; 43 weeks, P = 0.0207; 52 weeks, P = 0.0095. (b) Concurrently with the late-onset disease, the tamoxifen-treated DTA mice showed significant weight loss as compared to control littermate mice. Control mice: 32 weeks, n = 5; 33 weeks, n = 10; 34–35 and 43–45 weeks, n = 11; 36, 41 and 42 weeks, n = 14; 37–40 weeks, n = 15; 46–51 weeks, n = 9; 52 weeks, n = 7. DTA mice: 32 weeks, n = 4; 33–34 weeks, n = 10; 35 and 41 weeks, n = 12; 36–39 weeks, n = 16; 40 weeks, n = 15; 42 weeks, n = 11; 43 weeks, n = 9; 44 weeks, n = 8; 45–49 weeks, n = 6; 50–52 weeks, n = 5. Significance between control and DTA mice: 37 weeks, P = 0.021; 50 weeks, P = 0.0063; 51 weeks, P = 0.0063; 52 weeks, P = 0.0188. Data in a and b are presented as the mean ± s.e.m. *P < 0.05, **P < 0.01 and ***P < 0.001; two-way ANOVA with Bonferroni post hoc analysis.