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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Microglia pre-activation and neurodegeneration precipitate neuroinflammation without exacerbating tissue injury in experimental autoimmune encephalomyelitis

Fig. 5

MBP-EAE in LEWzizi mostly influences axonal damage but not pre-existing oligodendrocyte/myelin pathology. a, b Quantification of immunohistochemical stainings for Olig2 in the grey matter of the lumbar spinal cord (a) and mesencephalon (b) of 4-month-old (4 M) Lewis and LEWzizi rats at the peak (day 6; a, b) and during the recovery phase (day 10; a) of EAE. c, d Level of myelination assessed by densitometric analysis measuring integrated density of CNPase antibody labelling in the grey matter of the lumbar spinal cord (c) and mesencephalon (d) of 4 M Lewis and LEWzizi rats at day 6 (c, d) and day 10 (c) of EAE. e-h Quantification of cells with strong cytoplasmic accumulation of APP (e, f) or APP-positive neuronal spheroids and endbulbs (g, h) in the grey matter of the lumbar spinal cord (e, g) and mesencephalon (f, h) of 4 M Lewis and LEWzizi rats at the peak (day 6) of EAE. Graphs represent mean ± SD. Red lines indicate the mean ± SD of age-matched naïve Lewis or LEWzizi controls. Experimental groups comprise 6–8 rats each. Statistics result from two-way ANOVAs (separate analyses for day 6 and day 10) reporting (i) differences between Lewis EAE rats and LEWzizi EAE rats by black bars and (ii) differences between naïve controls rats and EAE rats by orange bars. Data were pooled according to rat genotype and independent of T cell genotype. *, p-value < 0.05; **, p-value < 0.01; ***, p-value < 0.001; ****, p-value < 0.0001; ns, not significant

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