Diminished amyloid-β uptake by mouse microglia upon treatment with quantum dots, silver or cerium oxide nanoparticles: Nanoparticles and amyloid-β uptake by microglia

Alzheimer's disease (AD) is a chronic neurodegenerative disease leading to progressive dementia in elderly people. The disease is characterized, among others, by formation of amyloid-beta (A beta) polypeptide plaques in the brain. Although etiology of the disease is not fully understood, recent research suggest that nanomaterials may affect AD development. Here, we described the consequences of exposure of mouse BV-2 microglia to silver nanoparticles (AgNPs, 50 mu g/mL), cerium oxide nanoparticles (CeO(2)NPs, 100 mu g/mL), and cadmium telluride quantum dots (CdTeQDs, 3 or 10 mu g/mL) in the context of its ability to clear A beta plaques. The brain microglial cells play an important role in removing A beta plaques from the brain. Cell viability and cycle progression were assessed by trypan blue test and propidium iodide binding, respectively. The uptake of A beta and NPs was measured by flow cytometry. Secretion of proinflammatory cytokines was measured with the use of cytometric bead array. A beta (0.1 mu M) did not affect viability, whereas NPs decreased microglia growth by arresting the cells in G1 phase (CdTeQDs) or in S phase (AgNPs and CeO(2)NPs) of cell cycle. The uptake of A beta was significantly reduced in the presence of AgNPs and CeO(2)NPs. In addition, the least toxic CeO(2)NPs induced the release of proinflammatory cytokine, tumor necrosis factor alpha. In summary, each of the NPs tested affected either the microglia phagocytic activity (AgNPs and CeO(2)NPs) and/or its viability (AgNPs and CdTeQDs) that may favor the occurrence of AD and accelerate its development.