Figure 3. Astrocyte‐specific Stat3 deletion reduces Aβ plaque burden and Aβ levels without altering APP metabolism.

• A, B
  Aβ plaque burden, as assessed by plaque load and size using an anti‐Aβ antibody, was strongly reduced in APP/PS1‐Stat3KO versus APP/PS1‐Stat3WT mice (*P < 0.05, Mann–Whitney test; scale bar, 300 μm).
• C
  Plaque density, assessed by staining brain sections with thioflavin (yellow), remained unchanged in APP/PS1‐Stat3KO versus APP/PS1‐Stat3WT mice (Mann–Whitney test; scale bar, 250 μm).
• D, E
  Electrochemiluminescence ELISA after sequential extraction from whole‐brain homogenates using RIPA and SDS buffer revealed that soluble Aβ_1–42 and Aβ_1–40 were significantly reduced (*P < 0.05, Mann–Whitney test), whereas there was a nonsignificant trend toward reduced levels of insoluble Aβ_1‐42 and Aβ_1‐40 (Mann–Whitney test).
• F–H
  Western blot quantification of full‐length amyloid precursor protein (APP) and its C‐terminal fragments (CTF) showed no differences between both groups (Mann–Whitney test).

Data information: Data are represented as mean ± SEM. For all datasets, n = 9 male mice for both groups (age, 11 months).Source data are available online for this figure.