Fig. 1.

a, b Minocycline treatment reduces microglia activation in APP/PS1 mice. The treatment reduced the numbers of Iba+ microglia in the dentate gyrus of APP/ PS1 mice to non-tg controls levels as well as decreased CD11b-immunoreactivity (IR) in the hippocampus of APP/PS1 mice. d, e Minocycline did not significantly reduce the levels of TNF-α, but downregulated the concentrations of IL-6 (p = 0.06). f The anti-inflammatory treatment was also associated with higher levels of the anti-inflammatory cytokine IL-10 (p = 0.07), (n = 5 per group/cytokine). c The number of Iba1+ microglia positively correlated with levels of IL-6. g–n Photomicrographs of immunofluorescent triple-labeled hippocampi show total microglia (Iba1 – green), activated microglia (CD11b – red), astrocytes (GFAP – blue) and respective overlay for APP/PS1 (g–j), and for APP/PS1 minocycline-treated mice (k–n). Insets in h and l represent high-magnification details of CD11b+ microglia selected by the yellow squares. o Western blot analysis of cortical samples to measure the levels of inflammation-driven protein iNOS in non-tg and APP/PS1 animals (middle lane). The same blot was then reprobed with anti-β amyloid antibody 6E10 to confirm the presence of the human APP transgene in these samples (upper lane). Equal protein loadings were confirmed by measuring GAPDH (lower lane). There was a significant decrease in densitometric values of iNOS protein in brain homogenates of APP/PS1 mice treated with minocycline. Scale bars = 60 µm (g–n) and 5 µm (insets). Dashed lines depict the SGZ. OML = Outer molecular layer. Error bars represent SEM. * p < 0.05, ** p < 0.01, ANOVA followed by Bonferroni post hoc test, Mann-Whitney U test and Spearman correlation.