Fig. 1

Infusion of blood from old Tg2576 mice accelerates Aβ deposition in young mice. a Representative pictures of amyloid deposits in the cortical area stained with the 4G8 anti-Aβ antibody and Thioflavin S (ThS). The scale bar corresponds to 20 µm. b The number of Aβ reactive plaques was counted and expressed as number of plaques per mm² of brain area analyzed. c The area of antibody-reactive Aβ deposits in each group was measured and divided by the total brain area (hippocampus and cortex region) analyzed (Aβ burden). The values are expressed as a percentage and multiplied by 1000. d The signal of ThS reactive deposits was measured as the stained area in relation to the total brain area (hippocampus and cortex region) analyzed (ThS burden) and was expressed as percentage. The quantity of insoluble Aβ₄₀ (e) and Aβ₄₂ (f) was measured using ELISA kits designed to specifically detect each of these variants. The values showed in the graphs displayed in panels b–f are expressed as mean ± SEM of the different animals used in each group (n = 5–6). For statistical analysis we did not consider the group of wild type animals injected with Tg2576 blood, since all these values were 0. *P < 0.05; **P < 0.01; ***P < 0.001 based on ANOVA followed by the Tukey’s multiple comparison post hoc test. In panels b–f the dotted line represents the threshold value used to calculate attack rate, i.e. the proportion of individual animals having significantly higher pathology than controls as explained in “Materials and methods” section. The numbers on top indicate the ratio of animals over the threshold/total number of animals in the group