Microglia are the resident macrophage-like cells of the CNS and are partly responsible for the clearance of amyloid-beta (Aβ) in the healthy brain. They display similar properties to peripheral macrophages and therefore they are phagocytic and capable of cytokine production. Alzheimer’s Disease (AD) is a common age-related neurodegenerative disease characterised by the formation of insoluble amyloid plaques that are associated with activated microglia, but it is unknown whether these microglia are involved in phagocytosis. Here we set out to assess whether phagocytic activity was altered in cells prepared from aged, compared with young, rats and to evaluate whether Aβ modulated phagocytic activity in these cells. We investigated phagocytic activity in rat primary CD11b-positive cells using flow cytometry to assess uptake of quantum dots and found pre-treatment with Aβ1-42 (2µM, 24h) exerted no significant effect on uptake. Phagocytosis of quantum dots (QD) was significantly decreased by pre-treatment of cells with H2O2 (**p<0.01; ANOVA; n=18) or NaF (***p<0.001; ANOVA; n=18). Phagocytosis was significantly increased in CD11b-positive cells prepared from aged, compared with young, rats (*p<0.05; Student’s t-test; n=26). We investigated microglial activation in brain tissue prepared from the same rats and found that there was a significant age-related increase in CD11b mRNA expression in both the hippocampus (*p<0.05; Student’s t-test; n=7) and the cortex (*p<0.05; Student’s t-test; n=7), while CD40 mRNA expression was significantly increased in hippocampus (***p<0.001; Student’s t-test; n=7). Expression of a lysosomal membrane protein, CD68, which is upregulated during phagocytic activity was also significantly increased in the hippocampus (**p<0.01; Student’s t-test; n=7) and the cortex of aged, compared with young, rats (**p<0.01; Student’s t-test; n=7). We investigated the effect of Aβ1-42 treatment on phagocytic activity of CD11b-positive cells prepared from brain tissue of aged, compared with young, rats and found differential age-related effects. Treatment of cells prepared from young rats with Aβ1-42 significantly increased phagocytic activity (*p<0.05; Student’s t-test; n=27) but Aβ1-42 induced no further increase in the phagocytic activity of cells isolated from the brains of aged rats. The data suggest that that the age-related increase in microglial activation is associated with an increase in phagocytic activity and that microglial cells prepared from aged rats cannot be further stimulated to increase their phagocytic activity by Aβ1-42.