Figure 2
From: Mechanisms of amyloid-β34 generation indicate a pivotal role for BACE1 in amyloid homeostasis
Aβ34 levels in AD post-mortem brain and in mouse brain tissue correlated with altered BACE1 expression and enhanced Aβ40 and Aβ42 levels. Expression of APP and BACE1, and Aβ34, Aβ40 and Aβ42 levels from post-mortem temporal brain and mouse cortices homogenates were analyzed by Western blot and MSD assays, respectively. Uncropped blots are included in a Supplementary Information file. Representative Western blot for the examination of APP and BACE1 expression levels (a). Quantification of relative protein amounts of APP (b) and BACE1 (c) of AD and non-AD. Absolute amounts of Aβ34 (d, g, and j), Aβ40 (e, h, and k) and Aβ42 (f, i, and l) determined with MSD 4-plex assays. For BACE1 knockout mice, cortices of 6 months-old 3 females and 3 males (g–i) and for London APP Transgenic mice, cortices of 6 months-old 7 females and 3 males (for WT) and 4 females and 3 males (for transgenic) (j–l) were analyzed. Data (b–f) were analyzed using unpaired Welch’s t-tests (due to violations of the normality assumption). Bars and error bars indicate mean ± s.e.m. (b) t(7) = 0.84, (c) t(13) = 3.34, (d) t(20) = 2.71, (e) t(18) = 2.54, (f) t(21) = 13.42. Data (d–f and j–l) were analyzed by unpaired t-test. Data (g–i) were analyzed by 1-WAY ANOVA and Tukey’s post-hoc tests were performed for pairwise comparisons; selected comparisons are highlighted ***p < 0.001, **p < 0.01, *p < 0.05. (g) Aβ34, 1-WAY ANOVA, F(2,15) = 10.33, p = 0.0015, (h) Aβ40, 1-WAY ANOVA, F(2,15) = 11.75, p = 0.0009, (i) Aβ42, 1-WAY ANOVA, F(2,15) = 6.637, p = 0.0086.
