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

• Published in: Human & experimental toxicology 2020-02, Vol.39 (2), p.147-158
• Main Authors: Sikorska, K, Grądzka, I, Sochanowicz, B, Presz, A, Męczyńska-Wielgosz, S, Brzóska, K, Kruszewski, MK
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Brain; Cadmium; Cadmium telluride; Cadmium tellurides; Cell cycle; Cell viability; Cerium; Cerium oxides; Cytokines; Dementia disorders; Etiology; Flow cytometry; G1 phase; Geriatrics; Inflammation; Iodides; Microglia; Microglial cells; Nanomaterials; Nanoparticles; Nanotechnology; Neurodegenerative diseases; Older people; Phagocytes; Polypeptides; Propidium iodide; Quantum dots; S phase; Senile plaques; Silver; Tumor necrosis factor-α
• ISSN: 0960-3271; 1477-0903
• DOI: 10.1177/0960327119880586

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-β (Aβ) 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 µg/mL), cerium oxide nanoparticles (CeO2NPs, 100 µg/mL), and cadmium telluride quantum dots (CdTeQDs, 3 or 10 µg/mL) in the context of its ability to clear Aβ plaques. The brain microglial cells play an important role in removing Aβ plaques from the brain. Cell viability and cycle progression were assessed by trypan blue test and propidium iodide binding, respectively. The uptake of Aβ and NPs was measured by flow cytometry. Secretion of proinflammatory cytokines was measured with the use of cytometric bead array. Aβ (0.1 μM) did not affect viability, whereas NPs decreased microglia growth by arresting the cells in G1 phase (CdTeQDs) or in S phase (AgNPs and CeO2NPs) of cell cycle. The uptake of Aβ was significantly reduced in the presence of AgNPs and CeO2NPs. In addition, the least toxic CeO2NPs induced the release of proinflammatory cytokine, tumor necrosis factor α. In summary, each of the NPs tested affected either the microglia phagocytic activity (AgNPs and CeO2NPs) and/or its viability (AgNPs and CdTeQDs) that may favor the occurrence of AD and accelerate its development.