Early Aggregation Kinetics of Alzheimer’s Aβ16–21 in the Presence of Ultrafine Fullerene Particles and Ammonium Nitrate

Abstract

One of the environmental health and safety concerns is the toxicological impact of ultrafine particles (UFPs) and secondary inorganic ions on human health, particularly on the development of neurodegenerative diseases. According to recent research studies, UFPs can be absorbed to human blood and have a toxicological effect on human organs. Due to their small particle size, UFPs can translocate to the human brain and contribute to the progression of neurodegenerative diseases. In this work, a molecular dynamics study was performed to investigate the impact of carbon-based UFP, mimicked by fullerene C60 molecule, on the aggregation of amyloid β (Aβ) peptides, which is related to the progression of Alzheimer’s disease. Moreover, the synergistic effect of the UFP and environmental pollutants was analyzed at various concentrations of the ions found in the environmental realm. In particular, the effect of C60 on the aggregation kinetics of eight Aβ16–21 peptides, the segment of Aβ peptide, was studied in the presence of NH4NO3 by varying the salt concentrations from 50 to 150 mM. Overall, the results showed the formation of large amounts of β-sheets in the systems with a slow initial rate of the aggregation of Aβ16–21 peptide octamer. In the absence of the UFP, the slowest initial rate of the aggregation of Aβ16–21 peptide octamer was observed at 50 mM salt concentration, while, in the presence of C60, the slowest aggregation kinetics of Aβ16–21 peptides was observed at 150 mM salt concentration. Moreover, in general, the presence of carbon-based UFP reduced the interpeptide interactions and decreased the initial rate of the aggregation of peptides due to the binding of peptides to C60.