| Summary: | Microglial cells clear the brain of pathogens and harmful debris, including amyloid-β (Aβ) deposits that are formed during Alzheimer’s disease (AD). We studied the expression of Msr1, Ager and Cd36 receptors involved in Aβ uptake and expression of Cd33 protein, which is considered a risk factor in AD. The effect of silver nanoparticles (AgNPs) and cadmium telluride quantum dots (CdTeQDs) on the expression of the above receptors and Aβ uptake by microglial cells was investigated. Absorption of Aβ and NPs was confirmed by confocal microscopy. AgNPs, but not CdTeQDs, caused a decrease in Aβ accumulation. By using a specific inhibitor—polyinosinic acid—we demonstrated that Aβ and AgNPs compete for scavenger receptors. Real-time PCR showed up-regulation of <i>Cd33</i> and <i>Cd36</i> gene expression after treatment with CdTeQDs for 24 h. Analysis of the abundance of the receptors on the cell surface revealed that AgNP treatment significantly reduced the presence of Msr1, Cd33, Ager and Cd36 receptors (6 and 24 h), whereas CdTeQDs increased the levels of Msr1 and Cd36 (24 h). To summarize, we showed that AgNP uptake competes with Aβ uptake by microglial cells and consequently can impair the removal of the aggregates. In turn, CdTeQD treatment led to the accumulation of proinflammatory Cd36 protein on the cell surface.
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