FIGURE 8.

Lack of apoA-I increases CAA in 6- and 12-month-old APP/PS1 mice. A and B, blood vessels were isolated from cortices and hippocampi of 12-month-old APP/PS/KO and APP/PS/WT mice, and insoluble Aβ was extracted using formic acid. Aβ₄₀ (A) and Aβ₄₂ (B) levels were measured by ELISA as described under “Experimental Procedures.” n = 8–10 mice/group. C, nonparametric analysis demonstrates negative correlation between Aβ₄₀ in blood vessels and cognitive performance. Spearman coefficient r = −0.54, p < 0.05. D, CAA is increased in the brains of 6- and 12-month-old mice APP/PS/KO mice as compared with age-matched APP/PS/WT. Amyloid deposits in cerebral blood vessels (cortex and hippocampus) were evaluated using X-34 staining as described under “Experimental Procedures.” For 6-month-old mice, n = 10; for 12-month-old mice, n = 13–14/group. E, representative images from 12-month-old APP/PS/KO mice and APP/PS/WT mice. The arrows point to blood vessels affected by CAA, and arrowheads point to the parenchymal deposits. Note that APP/PS/KO mice and APP/PS/WT mice have similar amounts of parenchymal plaques, but APP/PS/KO mice have more CAA. F, confocal laser microscope images of CAA in APP/PS/WT and APP/PS/KO mice. Blood vessels are delineated with smooth muscle actin antibody, and compact amyloid plaques are shown with X34 staining. Error bars, S.E.