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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer’s disease mutations but not by inhibition of BACE1

Fig. 5

Hippocampal indicators of epileptiform activity. a–e Coronal brain sections were obtained from genetically modified mice (+) and WT controls (−) at 3–5 (a–d) or 10–14 (a, e) months of age and immunostained for calbindin (a, b), neuropeptide Y (NPY) (a, c), or c-Fos (a, d, e). a Photomicrographs depicting typical levels and distributions of calbindin, NPY and c-Fos immunoreactivities in the hippocampus and dentate gyrus from mice of the indicated genotypes and ages. Arrows indicate depletion of calbindin in the molecular layer of the dentate gyrus (top) and increased NPY labeling of mossy fibers (middle) of a J20 mouse, and a 3-fold magnified inset image of c-Fos-positive granule cells (bottom) representing the boxed area in the dentate gyrus of a WT control. Scale bars: 500 μm (top and middle row), 200 μm (bottom row). b–e Quantitation of calbindin levels in the molecular layer of the dentate gyrus (b), NPY levels in the hilus of the dentate gyrus (c), and c-Fos-positive cells in the granular layer of the dentate gyrus (d, e). For each antigen, levels in genetically modified mice were expressed relative to mean levels in WT controls from the same line, which were defined as 1.0. n = 7–15 mice per group. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. WT from same line or as indicated by brackets, based on multiple Welch t-tests with Holm-Sidak correction (b, c), Kruskal-Wallis test with Dunn correction (d), or one-way ANOVA with Holm-Sidak correction (e). Values are means ± SEM

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