Elevated amyloid-β plaque deposition in dietary selenium-deficient Tg2576 transgenic mice

Selenium-containing proteins (e. g., glutathione peroxidases) are important antioxidants in neuronal defense against oxidative stress. In this study, the production of amyloid-beta (A beta) plaques in the brain of the Tg2576 transgenic mice was investigated under dietary selenium-deficient conditions. The 16-weekold mice were fed a selenium-deficient diet (0.004 mu g-selenium g(-1)-diet) or a selenium-adequate diet (0.386 mu g-selenium g(-1) diet) for 76 weeks. The selenium concentrations of the organs/tissues in the selenium-deficient diet-fed mice were significantly decreased in comparison to those in the selenium-adequate diet-fed mice; 1.7% of that in the selenium-adequate diet-fed mice in the liver and 43% of that in the selenium-adequate diet-fed mice in the brain. The A beta plaques formed in the brain were fluorescently stained with thioflavin T, and then the obtained images of the brain slices were qualitatively analyzed. The feeding of the selenium-deficient diet to the Tg2576 transgenic mice resulted in more than a two-fold increase in the total area of the A beta plaques in comparison to that of the selenium-adequate diet. The elevated A beta plaque deposition in the selenium-deficient mice can be explained as a consequence of decrease in the selenium concentration, which suggests that the selenium status is associated with the production and/or the clearance of the A beta peptide. The selenium-deficiency could possibly promote the onset and/or progression of Alzheimer's disease (AD) dementia, if the A beta peptides initiate a sequence of events that lead to AD dementia. Consequently, the results shown here suggest that AD has an important relation with the selenium status in vivo.