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. 2019 Dec 16;116(52):27074–27083. doi: 10.1073/pnas.1906358116

Fig. 8.

Fig. 8.

Demyelination and remyelination of ON are significantly correlated with VEP latency. (A) Myelin thickness measurements show significant difference in the g ratio in the core and subpia of the ONs during active disease, after recovery, and in control (active disease, n = 2; recovery, n = 3; control, n = 3; n ∼ 11,500 axons counted; multiple linear regression test, P < 0.0001). (B) Quantitative scoring of the myelin status shows a significant increase in remyelination along the ONs after recovery compared to ONs during active disease (active disease, n = 5; recovery, n = 3; 2-way ANOVA with Tukey’s multiple-comparisons posttest, P = 0.0002). Error bars show SD. (C) A gradual change in the myelin thickness was seen from levels 2 to 4 in partially recovered animals (n = 2 animals, n = 4,097 axons counted, multiple linear regression test, P < 0.0001). (D) Myelin status of the ON and VEP latency are significantly correlated (n = 5; simple linear regression test, r = 0.937; P = 0.006). The VEPs latencies of 2 animals from the active disease group with low remyelination status were highly delayed but unscorable; these are marked by # in the plot but were excluded from statistical regression analysis.