LAUSR

The complex pathogenic mechanisms of Alzheimer's disease (AD) include the aggregation of β-amyloid peptides (Aβ) into oligomers or fibrils as well as Aβ-mediated oxidative stress, which require comprehensive treatment. Therefore, the inhibition of Aβ aggregation and free-radical scavenging are essential for the treatment of AD. Nanoparticles (NPs) have been found to influence Aβ aggregation process in vitro. Herein, we report the inhibition effects of molybdenum disulfide (MoS2) NPs on Aβ aggregation. Polyvinylpyrrolidone-functionalized MoS2 NPs were fabricated by a pulsed laser ablation method. We find that MoS2 NPs exhibit multifunctional effects on Aβ peptides: inhibiting Aβ aggregation, destabilizing Aβ fibrils, alleviating Aβ-induced oxidative stress, as well as Aβ-mediated cell toxicity. Moreover, we show that MoS2 NPs can block the formation of the Ca2+ channel induced by Aβ fibrils in the cell membrane for the first time. Thus, these observations suggest that MoS2 NPs have great potential for a multifunctional therapeutic agent against amyloid-related diseases.