A suppressive effect of selenium on amyloid-β plaque deposition in Tg2576 transgenic mice brain

Abstract

Alzheimer’s disease (AD) is a chronic neurodegenerative disease and characterized by deposition of the amyloid-β (Aβ) peptide in the brain. Reactive oxygen species (ROS) are thought to be associated with the onset and/or progression of AD. Selenium-dependent glutathione peroxidases (GPxs) play a critical role in the brain in the extinction of ROS. The selenium concentration in the brain is kept higher than those of other organs/tissues even when dietary selenium is limited, which suggests the importance of this element in the brain. We previously reported that a dietary selenium deficiency caused the elevated deposition of Aβ plaques in the brain of Tg2576 transgenic mice, which is frequently used as a model of AD. In this study, we analyzed the GPx activity and lipid peroxidation of brain tissues after the feeding of a selenium-deficient diet to Tg2576 transgenic mice. We also investigated the effect of seleno-l-methionine (SeMet) supplementation on the Aβ plaque deposition in the brain. After feeding for 72 weeks, the selenium concentration and GPx activity in the brain of the selenium-deficient diet-fed mice was lower than those in the selenium-adequate diet-fed mice and SeMet-supplemented diet-fed mice. The deposition of Aβ plaques and lipid peroxidation in the SeMet-supplemented diet-fed mice brain appeared to decrease compared to those in the selenium-deficient diet-fed mice. Supplementation of SeMet might have a suppressive effect on the brain Aβ plaque deposition in theTg2576 transgenic mice.

Full Text PDF