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

• Published in: General physiology and biophysics 2024-11, Vol.43 (6), p.535
• Main Authors: Esmekaya, Meric A, Ertekin, Burhan
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Amyloid beta-Peptides - toxicity; Animals; Cell Line; Cell Survival - drug effects; Coffee - chemistry; Dose-Response Relationship, Drug; Exosomes - drug effects; Exosomes - metabolism; Hippocampus - cytology; Hippocampus - drug effects; Membrane Potential, Mitochondrial - drug effects; Mice; Nanoparticles - chemistry; Neurons - drug effects; Neurons - metabolism; Neuroprotective Agents - pharmacology; Peptide Fragments - toxicity
• ISSN: 0231-5882
• DOI: 10.4149/gpb_2024025

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.