CCL2 and Alzheimer disease: A different double transgenic model (Tg2576 × Tg1) in the same study found that, at a younger age, F4/80 and MCP-1 immunoreactivity was significantly less than at a higher age of 27 months leading them to conclude that this was due to progression of AD and that the MCP-1 but not F4/80 immunoreactivity in the intermediate aged mice represented a relatively early stage of inflammation prior to microglial activation.