Fig. 6

Less axonal loss in the acute disease phase in Wld ^S mutant mice. SC cross sections of Wld ^S mutant and WT mice with EAE were stained with anti-SMI31 antibody (a) and Bielschowsky’s silver impregnation (b) showing axonal loss in white matter lesions 20 days (acute) and 40 days (chronic) after disease onset. Quantification of SMI31⁺ phosphorylated axons revealed that the densities of intact healthy axons were significantly higher in Wld ^S mice as compared to WT mice in acute stage disease (a i–ii, c). However, similarly dense SMI31⁺ profiles were observed in the chronic stage (a iii–iv; lateral funiculus, c). Densities of SMI31⁺ profiles significantly decreased in both Wld ^S and WT mice from the acute to the chronic disease stage (a, c). Similarly, Bielschowsky’s silver impregnation displayed significantly higher relative axonal densities in Wld ^S mice only in the acute stage (b i–ii, d); again, axonal loss in Wld ^S mice was significantly more pronounced in the chronic than in the acute disease stage (b, d). Yellow and red boxes in (a i–ii) are higher magnifications of lesion areas with SMI31 immunostaining in acute disease. Error bars=SEM, n = 15 animals per group, *p < 0.05. Scale bars=(a i–ii) 100 μm; (a iii–iv, b i–ii) 150 μm; (b iii–iv) 200 μm; (insets a i–ii) 25 μm