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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Neurobiol Aging. 2010 Jan 6;32(11):1949–1963. doi: 10.1016/j.neurobiolaging.2009.12.010

Figure 3.

Figure 3

The age-related increase in Aβ1–42 accumulation and plaque formation was accompanied with the decrease in IDE protein expression in the hippocampus of 3xTg-AD female mice. (A) A total of 20 hippocampal sections collected at 210 μM intervals from one hemisphere of 3, 6, 9, 12 and 18-month-old 3xTg-AD female mice were stained with the Campbell-Switzer silver stain, which labels diffuse plaques in black and a more mature form of plaques in amber. (Left) Montage images revealed the temporal-spatial pattern of plaque formation that began and was concentrated in the subicular region in 12-month-old AD mice, which was significantly increased in 18-month-old AD mice. (Right) Upper panel: 10x views of plaque formation in the subicular region; Lower panel: 40x close-up views of a mature form of plaques stained in amber observed in 18-month-old AD mice. (B) ELISA data revealed an age-related increase in Aβ1–42 accumulation in the hippocampus of 3xTg-AD female mice; ** P < 0.01. (C) Western blot data revealed an age-related overall reduction in IDE protein expression in the hippocampus of 3xTg-AD female mice. Data are presented as the percent of IDE expression in 3-month-old AD mice; # P < 0.05 and ## P < 0.01 compared to 18-month-old mice; * P < 0.05 compared to 12-month-old mice; ** P < 0.01 compared to 3, 6, and 9-month-old mice; (D) Immunohistochemical staining revealed changes in immunoreactivity for Aβ (green) and IDE (red) that are consistent with observations from ELISA and Western blot analyses. β-tubulin was used as the loading control. Data are expressed as group mean ± S.E.M., n ≥ 4.