B-Amyloid treatment does not enhance the age-related increase in phagocytic activity of microglial cells

Abstract

Microglia are the resident immune cells of the brain and are activated following insult; activated microglia are acknowledged as having both beneficial and detrimental effects. In the healthy brain, microglia are responsible for surveillance and play a role in homeostasis; it is believed that they are also responsible for the clearance of Aβ. In Alzheimer's Disease, activated microglia are associated with insoluble amyloid plaques but it is unclear whether they are involved in Aβ clearance. We investigated uptake of quantum dots by microglia, as a measure of their phagocytic activity, using flow cytometry. There was no effect of Aβ on the phagocytic activity of mixed glial cultures or bone marrow derived macrophages but it significantly increased IL-1β production in both cells. Phagocytic activity was also assessed in cells isolated from the brains of young and aged rats and the data indicated that there was a significant increase in the phagocytic activity of CD11b+ cells isolated from the brains of aged, compared with young, rats. Treatment of cells prepared from young rats with Aβ significantly increased phagocytic activity but Aβ induced no further increase in the phagocytic activity of cells isolated from the brains of aged rats. The data suggest that microglial cells in the aged brain cannot be further stimulated to increase their phagocytic activity following an additional insult with Aβ.