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Fig. 2 | Molecular Neurodegeneration

Fig. 2

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. 2

Aβ and Aβ oligomer levels. a, b Overall levels of Aβ1-x and Aβ1–42 (a) and Aβ1–42/Aβ1-x ratios (b) in the hippocampus and cortex were determined by ELISA in 2–3-month-old mice of the indicated genotypes. (c) Relative hippocampal and cortical Aβ oligomer levels were determined in PBST fractions from 2 to 3-month-old I5, J20 and KI mice by 3D6/3D6 MSD ELISA. Based on a comparison of WT and App−/− mice (Additional File 1: Fig. S4e), the average electrochemiluminescence (ECL) signal in WT controls was considered background and subtracted from ECL signals obtained in individual genetically modified mice. n = 5–12 mice per group. *P < 0.05, **P < 0.01, **** P < 0.0001 vs. I5 or as indicated by brackets, based on multiple Welch t-tests with Holm-Sidak correction (a, b) or one-way ANOVA and Holm-Sidak correction (c). Values are means ± SEM

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Molecular Neurodegeneration

ISSN: 1750-1326