Fig. 6

Quantitative analysis of amyloid β protein (Aβ) pathology and biochemical studies in R1.40 mice. Quantitative analysis of the Aβ pathology of the R1.40 mice injected with human brain extracts from the Alzheimer’s disease (AD) (R1.40 mice-AD), cerebral amyloid angiopathy (CAA) (R1.40 mice-CAA), AD + CAA (R1.40 mice-AD + CAA), and less Aβ pathology groups (R1.40 mice-less Aβ), and PBS (R1.40 mice-PBS) (A–D). Concentrations of Aβ40, Aβ42, and Aβ40 + Aβ42, and ratio of Aβ40/Aβ42 in the mouse brain extracts (E–H) and in the mouse brain pellets (I–L). The Aβ load in the R1.40 mice-AD was significantly higher than that in the R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-PBS despite no significant difference in Aβ loads between R1.40-AD and R1.40 mice-less Aβ (A). The Aβ42 load was significantly higher in the R1.40 mice-AD than in all the other groups of R1.40 mice (C), while the Aββ40 load was not significantly different among them (B). CAA counts were not significantly different among the R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-less Aβ, although the CAA count in R1.40 mice-PBS was significantly lower than in all other mice groups (D). In the mouse brain extract, no significant difference in the concentrations of Aβ0, Aβ42, and Aββ40 + Aβ42 in the mouse brain extracts was observed among R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-less Aβ (E–G). Compared to R1.40 mice-PBS, concentrations of Aβ40 in R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-less Aβ; that of Aβ42 in R1.40 mice-AD; and that of Aβ40 + Aβ42 in R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40-less Aβ were significantly higher (E–G). The Aβ40/Aβ42 ratio of R1.40 mice-PBS was significantly higher than that of R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA and R1.40 mice-less Aβ, although the Aβ40/Aβ42 ratio was not significantly different among the 4 groups of R1.40 mice injected with human brain extracts (H). The Aβ40/Aβ42 ratios of all groups of R1.40 mice were Aβ40 dominant (H). In the mouse brain pellets, the concentrations of Aβ40, Aβ42, or Aβ40 + Aβ42 were not significantly different among R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-less Aβ (I–K), although the concentrations of Aβ40 + Aβ42 and Aβ42 in R1.40 mice-PBS were significantly lower than those in all other groups (I and K). The concentration of Aβ40 in R1.40 mice-PBS was significantly lower than that in R1.40 mice-CAA, R1.40 mice-AD + CAA, and R1.40 mice-less Aβ (J). The Aβ40/Aβ42 ratio of R1.40 mice-PBS was significantly higher than that of R1.40 mice-AD, R1.40 mice-CAA and R1.40 mice-AD + CAA, and the Aβ40/Aβ 42 ratio of R1.40 mice-AD was significantly lower than that of R1.40 mice-CAA and R1.40 mice-less Aβ (L). The Aβ40/Aβ42 ratio of all groups of R1.40 mice indicated Aβ40 dominance (L). *p < 0.01, **p < 0.05, ***p < 0.001