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Fig. 6 | Acta Neuropathologica Communications

Fig. 6

From: Low autophagy capacity implicated in motor system vulnerability to mutant superoxide dismutase

Fig. 6

Heterozygous deletion of Becn1 in hSOD1G93A mice enhances aggregation and shortens survival. a Kaplan-Meier curves for disease onset and survival of hSOD1G93A (n = 9; male:female 5:4) and hSOD1G93A/Becn1 +/- mice (n = 12; male:female 7:5). b Scatter plot for disease duration. Bars represents the mean values. **P < 0.01 (two-tailed Welch’s t-test). c Western blots for hSOD1G93A in whole homogenates, detergent-insoluble, and detergent-soluble fractions extracted from the spinal cords (n = 4 per genotype per disease stage). β-Actin in whole homogenates was used as a loading control. Amounts of (d) insoluble and (e) soluble hSOD1G93A protein. **P < 0.01 vs. disease stage-matched hSOD1G93A mice; N.S.: not significant vs. disease stage-matched hSOD1G93A (one-way ANOVA with Tukey-Kramer’s test). f Upper: Filter-trapped hSOD1G93A aggregates in the spinal cords of the mice (n = 4 per genotype per disease stage). Lower: Amounts of hSOD1G93A aggregates. **P < 0.01 vs. disease stage-matched hSOD1G93A (one-way ANOVA with Tukey-Kramer’s test)

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