Maysin plays a protective role against α-Synuclein oligomers cytotoxicity by triggering autophagy activation.

Parkinson's disease (PD) is a widespread neurodegenerative disorder characterized by the progressive loss of neurons. The accumulation of aggregated forms of the α-Synuclein (Syn) protein is the main cause of neurotoxicity in PD by disrupting cellular homeostasis until neuronal death. Scientific research is constantly looking for natural products as preventive agents against the progression of several neurodisorders due their safety and non-toxic nature. Neuroprotective phytochemicals include Maysin (Mys), the most abundant C-glycosilflavone in corn silk. In this work, the Mys protective role against damage by Syn amyloid aggregates - oligomers and fibrils - was investigated in SH-SY5Y human neuroblastoma cells obtaining novel and interesting information concerning the Mys molecular mechanism of action. Mys showed effectiveness in preventing the typical toxic events induced by Syn amyloid aggregates, i.e. oxidative stress and imbalance of intracellular calcium homeostasis. Mys exhibited a cytoprotective role, especially against Syn oligomers injury, activating an autophagic degradative process, thus playing a key role on several features of amyloid neurotoxicity. Therefore, Mys could be proposed for the first time to the scientific community as an interesting novel natural compound that might allow to develop alternative strategies to prevent the damage of Syn oligomers involved in Parkinson's disease.