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. 2024 Jun 18;134(16):e177692. doi: 10.1172/JCI177692

Figure 5. Neuronal VGF deficiency protects from neuroaxonal damage in EAE.

Figure 5

(A) EAE disease course of Snap25-Cre × Vgffl/fl (Vgf-cKO; n = 10) animals and respective Vgffl/fl (n = 11) control littermates. Points represent mean per group per day, additionally, SEM is shown. (B) Cumulative clinical score using AUC during acute (days 11–20), recovery (days 21–30), and chronic (days 31–40) disease stages of EAE. (C and D) Disease onset (C) and maximal disease score (D) of Vgf-cKO and control mice. (E) Number of HuC/D-positive neurons in the ventral horn spinal cords of WT (n = 5) and Vgf-cKO (n = 7) EAE mice 40 days after immunization. Scale bar: 50 μm. (F) Number of axons in dorsal columns of the cervical spinal cord assessed by SMI staining in Vgf-cKO (n = 9) and control mice (n = 10) undergoing EAE 40 days after immunization. Scale bar: 50 μm. (G) Quantification of luxol fast blue-positive axonal area per 100 μm2 in the dorsal columns of the cervical spinal cords of WT (n = 6) and Vgf-cKO (n = 8) EAE mice 40 days after immunization. Scale bar: 500 μm. Points represent individual experiments, additionally mean is shown. For comparing EAE phenotypes nonparametric Kolmogorov-Smirnov test was used. For IHC analyses unpaired t test was used. *P < 0.05.