Antioxidative stress effect of epicatechin and catechin induced by Aß25-35 in rats and use of the electrostatic potential and the Fukui function as a tool to elucidate specific sites of interaction.

Alzheimer's disease (AD) is a neurodegenerative disorder caused by the aggregation of the amyloid-beta peptide (Aß) in senile plaques and cerebral vasculature. The Aß25-35 fraction has shown the most toxicity; its neurotoxic mechanisms are associated with the generation of oxidative stress and reactive astrogliosis that induce neuronal death and memory impairment. Studies indicate that pharmacological treatment with flavonoids reduces the rate of AD, in particular, it has been shown that antioxidants are compounds that could interact with this peptide due to their antioxidant proprieties. In this study, experimental and computational tools were used to calculate the molecular electrostatic potential and the Fukui function with the Gaussian 09 computational program, to predict the most reactive parts of these molecules and make the complex between Aß25-35 and two flavonoids (catechin and epicatechin) in the absolute gas-phase, where a possible interaction between them was observed. This is important for understanding the Aß25-35-Flavonoid (A-F) interaction as a therapeutic strategy to inhibit the neurotoxic effects that this peptide causes in AD, which currently is still considered an ambiguous process.