Extended Data Fig. 3: APP levels and processing, neuritic dystrophy and astrocyte activation in 9-month-old APP23 animals.
From: Innate immune memory in the brain shapes neurological disease hallmarks
a, b, Micrograph of fluorescent staining for amyloid plaque (Methoxy-X04; green) and amyloid precursor protein (APP; red) (a) shows neuritic dystrophy surrounding the amyloid deposit, which is unchanged by LPS treatments (b; n = 5, 5, 5 animals). c, Overall Pearson’s correlation of plaque size with neuritic dystrophy (APP area; n = 49, 39, 42 plaques for PBS, 1 × LPS, 4 × LPS groups). d, Western blotting analysis (for gel source data, see Supplementary Fig. 1) of brain homogenates for APP and C-terminal fragment-β (CTFβ; n = 7, 4, 7 mice), and soluble APPβ ELISA (n = 6, 6, 6 mice). e, Micrograph of activated astrocytes (glial fibrillar acidic protein: GFAP) surrounding an amyloid plaque (Congo red) and quantification of the number of plaque-associated GFAP-positive astrocytes (n = 6, 6, 5 mice). Scale bar, 10 µm (a), 20 µm (e). Data are means ± s.e.m. *P < 0.05 for one-way ANOVA with Tukey correction.
