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. 2019 Jul 10;39(28):5562–5580. doi: 10.1523/JNEUROSCI.1760-18.2019

Figure 8.

Figure 8.

Increased NgR1 and putatively impaired CRMP2-depdent axonal transport in brain lysates of patients with progressive MS. A, Western immunoblot detection for (first row) NgR1 and (second row) actin loading control of brain lysates from NNDC, AD, FTD, HD, and secondary progressive MS. B, Densitometric quantification of the levels of NgR1 normalized to actin loading control (n = 4, mean ± SEM, one-way ANOVA with post Tukey's test; *p < 0.05). C, Immunoprecipitation of pCRMP2-T555 using polyclonal anti-pCRMP2-T555 antibody and probed with Kinesin light chain 1 (KLC-1) and α-tubulin. D, AD (n = 7), FTD (n = 9), HD (n = 4), and MS (n = 5) lysates have ∼90, 85, 80, and 70% decrease in the percentage of Kinesin-bound to CRMP2 compared with non-neurological disease control lysates, respectively. E, AD (n = 8), FTD (n = 9), HD (n = 4), and MS (n = 5) lysates exhibit an approximate 80, 60, 50, and 40% reduction in the percentage of α-tubulin-bound to CRMP2 compared with non-neurological disease control lysates, respectively (mean ± SEM, one-way ANOVA with post Tukey's test; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).