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Fig. 6 | Molecular Neurodegeneration

Fig. 6

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

Fig. 6

Bergmann glia specific IKK2-CA expression in the IKK2-CASept4 model recapitulates the cerebellar pathology of the GFAP.tTA/tetO.IKK2-CA mice. a Co-Immunostaining for the GFP reporter coexpressed with the IKK2-CA transgene and for Aldh1l1 as astrocyte marker shows co-localisation. Arrows indicate Bergmann glia cell bodies. Scale bar: 20 μm. b Immunostaining for GFAP shows intensly stained and unorganized Bergmann glia processes in the molecular layer indicating Bergmann glia activation in IKK2-CASept4 mice. Inlays: higher magnification of the GFAP channel in the molecular layer. Scale bars: 20 μm. c Immunoblotting for Mac2 indicates microgliosis, transgene expression (IKK 1/2 immunoreactivity) and induction of the NF-κB target Lcn2. d Sept4-Cre induced IKK2-CA expression results in macroscopic cerebellar atrophy at 28–29 weeks. Scale bar: 1 mm. e Quantification of maximal rostro-causal length of the cerebellum (single animals and mean); statistical analysis: 2-tailed unpaired t-test, *** p < 0.001. f Histological analysis of the simple lobule reveals loss of Purkinje cells in the IKK2-CASept4 model. Arrows: Purkinje cells. Scale bars: 100 μm (left panels); 20 μm (enlargements, right panels). g Quantification of Purkinje cell loss from Nissl stainings. Statistical analysis: 2-tailed unpaired t-test, * p < 0.05

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