Additional file 3: of Deregulation of neuronal miRNAs induced by amyloid-β or TAU pathology

Figure S2. Correlation between miRNA expression and pathology load in APPtg and TAUtg mice and AD patients. A) Hippocampal levels of soluble and insoluble Aβ40 and Aβ42 levels were measured by ELISA in APPwt and APPtg mice at 4 M and 10 M of age. 2-way ANOVA demonstrates significant effects for age, genotype and age*genotype for all measured Aβ species, with 10 M APPtg mice having significantly higher expression compared to all other groups. ***:p < 0.001 (Tukey’s post-hoc analysis). B) Spearman correlation with false discovery rate (FDR) p-value adjustment, demonstrate significant correlations (p < 0.05) between all miRNAs and all Aβ species. C) Representative western blot of total TAU and phosphorylated TAU (as measured by AT8 & AT270). D) Quantification of the blots shown in C), demonstrating significant genotype effects for both TAU and phosphorylated TAU. Levels of phosphorylated TAU are normalized to both β-actin as well as to TAU expression levels. E) Spearman correlation with FDR p-value adjustment between the 6 miRNAs of interest and levels of TAU protein and phosphorylated TAU. The correlation coefficient is only stated in the cells of the table if it was statistically significant (p < 0.05), otherwise the cell reads ‘0’. F) Spearman correlation with FDR p-value adjustment between the qPCR-based expression levels of the 5 expressed miRNAs in human tissue and the protein levels of TAU, phosphorylated TAU (AT8 & AT270), full length APP (flAPP), soluble APPβ (sAPPbeta) and APP c-terminal fragments (CTFs) as measured by western blotting in [31]. Only cells with significant (p < 0.05) correlations state the correlation coefficient, the others read ‘0’. (PNG 3343 kb)