Fig. 3

Phagocytosis of Tau oligomers and activation of microglia. a N9 microglia were incubated with extracellular Tau oligomers for 24 h to initiate phagocytosis. The immunostaining study analyzed the presence of A11⁺ microglia indicating the phenomenon of active internalization of oligomer overburden. b The number of A11+ microglia was equal in amount during the phagocytosis of hTau40^WT oligomers and fibrillar aggregates. c 3D localization studies have shown that the microglia have engulfed an adequate amount of Tau oligomers and low molecular weight aggregates (A11 staining) as compared to the untreated control group. d, e The quantification of total A11 intensity in microglia upon different Tau species treatment group and the A11 intensity per square area have defined the density of A11 fluorescence in treated microglia by ZEN 2.3 image analytical microscopic software. f, g Microglial activation is mediated by the peri-membrane localization of Ca²⁺ binding adaptor protein Iba1 in the case of preformed Tau aggregate treatment while the oligomer-treated group showed an increased level of cytosolic localization of Iba1 in microglia. The levels of Iba1 were quantified by ZEN 2.3 image analysis software in N9 microglia treated with Tau species. Significant at the mean difference between treatment groups (X − X`) > Tukey’s criterion (T)