Fig. 7

The effects of Ab-T1 on the number and activation status of plaque associated microglia. Ab-T1 induces an increase in the number of microglia activated in the vicinity of the plaques. a Hippocampus and cortex region representative micrographs of brain section of 5xFAD Alzheimer’s disease mice treated with Ab-T1 and control IgG (experiment 1). Black squares indicate an example of randomly selected 80 × 80 μm counting frame at × 20 magnification. b Enlarged images (× 20) of randomly selected frames from representative micrographs. c The average number of plaque associated-microglia in the hippocampus and cortex regions of treated mice. d A more efficient plaque coverage by a higher number of in situ associated microglia (average plaque-associated microglia; upper panels) based on different stages of microglia activation defined by their morphology (activated microglia—stage II and III) illustrated in the lower panels. (c, two-tailed student’s t test, **P = 0.0006, *P = 0.00024), (d, two-tailed student’s t test, *P = 0.0000028, **P = 0.00000065). Scale bar = 200 μm (a) and 50 μm (b). The immunohistochemistry studies were conducted employing double staining with anti-beta amyloid (4G8; red) and anti-Iba1 (brown) antibodies. e Confocal microscope images showing co-localization of CD68 with Iba1 positive cells in 5xFAD mice brain slices. f Ab-T1 but not control IgG augments BMDM induced proliferation. Cell proliferation was measured by flow cytometry (quantifying cell population growth). Results are mean of four repeated experiments with triplicate technical sample repetition