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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 4.

Figure 4

17β-E2 attenuated Aβ1–42 accumulation and plaque formation, which was accompanied with an increase in IDE protein expression, in the hippocampus of 12-month-old 3xTg-AD female OVX mice. (A) A total of 20 hippocampal sections collected at 210 μM intervals were stained with the Campbell-Switzer silver stain. The staining revealed a significant reduction in plaque formation in OVX mice treated with 17β-E2 compared to vehicle alone-treated OVX mice. (B) A significantly lower percentage of sections was affected by plaques in OVX mice treated with 17β-E2 compared to vehicle alone-treated OVX mice; * P < 0.05. (C) A significantly smaller area in the subicular region (defined by box 1) was occupied by plaques in OVX mice treated with 17β-E2 compared to vehicle alone-treated OVX mice; * P < 0.05. (D) ELISA data revealed a significant reduction in Aβ1–42 accumulation in the hippocampus of OVX mice treated with 17β-E2 compared to vehicle alone-treated OVX mice; * P < 0.05. (E) Western blot data revealed a significant increase in IDE protein expression in the hippocampus of OVX mice treated with 17β-E2 compared to vehicle alone-treated OVX mice; ** P < 0.01. (F) Consistent with ELISA and Western blot data, immunohistochemical staining revealed a lower intensity of Aβ immunoreactivity (green) and a higher intensity of IDE immunoreactivity (red) in hippocampal sections of OVX mice treated with 17β-E2 than showed in sections of vehicle alone-treated OVX mice. β-tubulin was used as the loading control. Data are expressed as group mean ± S.E.M., n ≥ 4.