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Fig. 8 | Acta Neuropathologica Communications

Fig. 8

From: Lipid microdomain modification sustains neuronal viability in models of Alzheimer’s disease

Fig. 8

Genetic GCS inhibition increases neuronal viability in a 5xFAD mouse model of Alzheimer’s disease. a The biosynthesis of the major neuronal a- and b-series gangliosides (outlined) is inhibited by Cre-mediated deletion of GCS under the inducible forebrain-specific CamKIIα promoter. b In situ hybridization shows that Ugcg mRNA is almost completely absent in hippocampal CA1 region of 5xFAD//Cre mice (scale bar: 200 μM). c Cresyl violet staining of cortical layers of 7 months old mice. A layer 5 pyramidal neuron is depicted (inset, arrowheads). Layer 1 thickness is reduced in 5xFAD mice, but maintained in 5xFAD//Cre mice (n = 21–27 measurements from 8–11 mice). Aβ plaques in cortical layer 5 are stained by the antibody 6E10. d Western blot of the neurodegeneration marker p25 indicates neurodegeneration in 5xFAD mice, which is less pronounced in 5xFAD//Cre mice (n = 8–10 mice). e Total IR in cortical neurons have been quantified by PLA using two different IR antibodies (N-20 and D-17) in 7 months old Ugcgf/f, 5xFAD, and 5xFAD//Cre mice. The PLA shows that the decrease in IR in 5xFAD mice is less pronounced in 5xFAD//Cre mice (n = 80–98 cells from 3–5 mice per group, scale bar: 10 μM). f PLA shows that IR/Cav-1 proximity is increased in cortical neurons of 7 months old 5xFAD mice, and comparable to controls in 5xFAD//Cre mice (n = 71–103 neurons from 3–5 mice per group, scale bar: 5 μM). Unpaired two-tailed student’s t-test (if p ≤ 0.05, p ≤ 0.01 or p ≤ 0.001, results are marked with (*), (**), or (***), respectively). Means ± SEM

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