Coenzyme Q10 Prevents Scopolamine Associated Hippocampal-Dependent Memory Deficits in Mice

Abstract

Scopolamine has been widely used to induce pharmacological model of memory impairment. Scopolamine impairs cognitive function via mitochondrial dysfunction and oxidative stress beyond that of direct cholinergic antagonism. Coenzyme Q10 (CoQ10), a mitochondrial component, protects mitochondria from reactive oxygen species and assist in energy production. Mitochondrial dysfunction appears with CoQ10 deficiency in the neurodegenerative disease. It is unknown whether CoQ10 can prevent scopolamine-associated spatial working memory deficits. We treated adult Swiss albino mice either by saline (control) or scopolamine or scopolamine plus CoQ10 or CoQ10 alone for four weeks and subsequently assessed spatial memory formation and locomotor activity. We euthanized mice to determine oxidative stress markers including lipid and protein oxidation, superoxide dismutase and catalase activity in brain tissues.Scopolamine-treated mice showed impaired spatial learning and memory formation. Scopolamine significantly increased levels of lipid peroxidation, reduced activity of superoxide dismutase and catalase compared to the controls. On the contrary, concomitant administration of scopolamine and CoQ10 did not cause spatial memory deficits. Furthermore, combined treatment did not alter hippocampal lipid and protein oxidation and activity of superoxide dismutase and catalase. Surprisingly, only CoQ10 supplementation improves oxidative stress markers compared to the control.Our results strongly suggest a protective ability of CoQ10 on spatial memory formation when concomitantly given with scopolamine in mice. The observed protective activity was presumably via an increased level of superoxide dismutase enzyme. We propose a further study to measure hippocampal mitochondrial function to reveal the underlying mechanism of CoQ10 before trial in humans.