Neuroprotective effects of coffee-derived exosome-like nanoparticles against Aβ-induced neurotoxicity.

Abstract

The present study aimed to provide experimental evidence that CDELNs (coffee-derived exosome-like nanoparticles) may be a candidate for the treatment or prevention of amyloid-β (Aβ)-induced Alzheimer's disease (AD). An in vitro Alzheimer's model was created with Aβ-induced toxicity in mouse hippocampal neuronal cells (HT-22). Aβ(1-42)-exposed cells were treated with different concentrations of CDELNs (1-50 μg/ml) and the viability of cells was analyzed. The change in the mitochondrial membrane potential (ΔΨm) of cells was also determined. CDELNs treatment increased the viability of Aβ(1-42 )-toxicity-induced HT-22 cells significantly. The increase in the viability of Aβ(1-42)-toxicity-induced cells was correlated with an improvement in ΔΨm. CDELNs treatment restored the dissipated ΔΨm. These results suggested that CDELNs protect neuronal cells against Aβ(1-42)-induced neurotoxicity by repairing mitochondrial dysfunction. CDELNs might be a useful neuroprotective agent for the treatment or prevention of Aβ-induced AD. Further animal and clinical studies should be carried out to investigate the neuroprotective potential of CDELNs against Aβ-induced AD.