Myricetin prevents high molecular weight Aβ_1‐42 oligomer‐induced neurotoxicity through antioxidant effects in cell membranes and mitochondria

Background Excessive accumulation of amyloid β-protein (Aβ) is one the primary mechanisms that leads to neuronal death with phosphorylated tau in pathogenesis Alzheimer’s disease (AD). Protofibrils, high-molecular-weight Aβ oligomers (HMW-Aβo), are implicated be important targets modifying therapy AD. We previously reported phenolic compounds such as myricetin inhibit Aβ1-40, Aβ1-42, and α-synuclein aggregations, including their oligomerizations, which may exert protective effects against AD Parkinson’s disease. The purpose this study was clarify detailed mechanism effect neurotoxicity HMW-Aβo SH-SY5Y cells. Method To assess on HMW-Aβo-induced oxidative stress, we systematically examined level membrane damage by measuring cell lipid peroxidation, fluidity, potential, mitochondrial evaluated permeability transition (MPT), reactive oxygen species (ROS), manganese-superoxide dismutase (Mn-SOD), adenosine triphosphate (ATP) assay Result Myricetin has been found increased viability suppression disruption cells, shown reducing phospholipid peroxidation increasing fluidity resistance. also suppress mitochondria dysfunction, demonstrated decreasing MPT, Mn-SOD, ATP generation, raising mitochondrial-ROS generation. Conclusion These results suggest preventing through multiple antioxidant functions developed a disease-modifying agent