Plasmon-activated water reduces amyloid-β42 aggregation and exhibits neuroprotective potential in Alzheimer’s disease

Background Alzheimer’s disease (AD) is the leading cause of dementia, yet effective therapies to prevent neuronal loss are lacking. Plasmon-activated water (PAW) has shown anti-inflammatory and cognitive-enhancing effects in previous studies, but its neuroprotective potential in AD remains underexplored. Methods A novel device was developed to generate PAW, which exhibited stable negative zeta potential and potent free radical scavenging activity (Fenton reaction and 2,2-Diphenyl-1-picrylhydrazyl radical assay, DPPH assays). In vitro, synthesized the 42-residue amyloid-β peptide (Aβ42) were used to analyze aggregation in PAW by Thioflavin T and transmission electron microscope (TEM). A secreted Aβ42 (hBRI-Aβ42)-expressing plasmid was constructed and transfected into Neuro-2a cells. Aβ42 expression and aggregation were confirmed by western blotting, immunostaining, green fluorescent protein (GFP) fluorescence, and Thioflavin S. In vivo studies used a zebrafish model expressing hBRI-Aβ42 under the HuC promoter. Significant findings PAW inhibited synthesized Aβ42 peptides aggregation in vitro. PAW-treated Neuro-2a cells exhibited reduced intracellular Aβ42 aggregation. In zebrafish, hBRI-Aβ42 expression caused neuronal loss without affecting survival. Notably, PAW treatment significantly mitigated neurotoxicity and preserved neuronal integrity. These results suggest that PAW exerts a neuroprotective effect by reducing Aβ42 aggregation and oxidative stress, supporting its potential as a preventive strategy for AD.