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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: Transient IKK2 activation in astrocytes initiates selective non-cell-autonomous neurodegeneration

Fig. 4

IKK2-CA expression in Bergmann glia disrupts their morphology in correlation with the stage of cerebellar degeneration. a Co-staining for hIKK2 (transgene) and the astrocyte marker Aldh1l1 at 20 weeks of age in a cerebellum without detectable degeneration (“early deg”) and in a late stage of degeneration (“late deg”) Arrows: Bergmann glia cell bodies. b-d IKK2-CA-expressing (hIKK2 positive) Bergmann glia marked by arrows display nuclear localization of RelA indicating active NF-κB signalling (b). Arrowheads: Purkinje cell bodies (hIKK2 negative). c Enlargement of the box in B. d Quantification of nuclear RelA immunofluorescence intensity in cells in the Purkinje cell layer, including IKK2-CA (hIKK2) expressing Bergmann glia. n = 360 cells of 3 control and n = 480 of 4 IKK2-CA animals. Statistical analysis: 1-way ANOVA with Tukey’s post-test, *** p < 0.001. e Staining for GFAP at 20 weeks of age shows Bergmann glia processes in the molecular layer. Controls and IKK2-CA cerebella without detectable degeneration (“early deg”) show parallel Bergmann glia processes with weak GFAP. Severely degenerated cerebella (“late deg”) show intensely stained, thickened and unorganized processes. f Occasionally, IKK2-CA animals without obvious Purkinje cell loss (age 12 weeks) show patches of Bergmann glia with increased GFAP expression and first signs of disorganisation. Merged images show DAPI co-staining (blue). Scale bars: 20 μm

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