Extended Data Fig. 2: Minor modulation of plaque load by peripheral stimuli and gut microbiota.
(a) Quantification of plaque number (left) and individual plaque sizes (right) of groups as shown in Fig. 3. Left: Each symbol represents one animal. Mean ± s.e.m. is shown. Right: Each symbol represents one analyzed plaque; N = 1,838 – 2,972 plaques per group. Median ± interquartile range is shown. Specific P values of statistical tests are indicated. (b) ELISA of human Aβ(1-42) peptides in soluble (left panel) and insoluble (right panel) fractions of cortices from untreated, ABX- and LPS-treated Cx3cr1CreERT2R26Confetti5xFAD+ animals at an early (untreated: n= 3, ABX: n=2, LPS: n = 4) and late stage (untreated: n= 3, ABX: n=3, LPS: n = 3) of disease. Each symbol represents one animal. Mean ± s.e.m. is shown. Specific P values of statistical tests are indicated. (c) Representative images of CD68+ PAM in untreated (upper panel) or ABX-treated (lower panel) Cx3cr1CreERT2R26Confetti5xFAD+ animals at an early stage of disease. Immunofluorescence for CD68 (magenta), Thioflavine-S (amyloid beta, cyan), Iba-1 (microglia, green) and DAPI (blue) is shown. Scale bar = 50 µm. (d) Quantification of the percentage of CD68+ area in Iba-1+ microglial cell bodies of untreated, ABX- and LPS-treated Cx3cr1CreERT2R26Confetti5xFAD+ animals at an early and late stage of pathology (all groups: n= 5) compared to untreated control littermates (n =4). Each symbol represents one animal. Mean ± s.e.m. is shown.Specific P values of statistical tests are indicated.
