Dementia and Alzheimers Disease

Biography

Biography: Abha Chauhan

Abstract

Amyloid beta-protein (Aβ) is the major protein of amyloid deposits in the brain of patients with Alzheimer’s Disease (AD). Extensive evidence suggests neurotoxic effects of Aβ and the role of oxidative stress and inflammation in AD. Walnuts are rich in components that have antioxidant and anti-inflammatory properties. Previous in vitro studies have shown that walnut extract inhibits Aβ fibrillization, solubilizes its fibrils, and has protective effects against Aβ-induced oxidative stress and cell death in PC12 cells. In the Tg2576 transgenic mouse model of AD (AD-tg), we have reported the beneficial effects of dietary supplementation of 6% (T6) or 9% walnuts (T9) [equivalent to 1 or 1.5 oz of walnuts per day in human] on the memory, learning skills anxiety and motor coordination when compared to AD-tg mice on diet without walnuts (T0). The diets for the experimental and control mice were comparable as regards to total calories and the contents of protein, carbohydrate, and fat. To understand the mechanism of beneficial effects of a diet with walnuts in AD, we have recently studied the effects of walnuts on Aβ levels and oxidative stress markers in AD mice. In AD-tg mice on diet with walnuts (T6, T9), the levels of soluble Aβ were lower in the brain and higher in the blood when compared to T0 mice, suggesting that walnuts in the diet can increase the clearance of Aβ from the brain to the blood. We also observed a significant decrease in free radical levels and oxidative damage (lipid peroxidation, protein oxidation) coupled with increased antioxidant status (superoxide dismutase, catalase, and glutathione peroxidase) in these T6 and T9 mice on diet with walnuts. In conclusion, these studies suggest that diet with walnuts may have beneficial effects in reducing the risk, delaying the onset, or slowing the progression of AD because walnuts can help to improve memory and learning skills, inhibit Aβ fibrillization and maintain Aß in the soluble form, decrease Aβ-induced oxidative stress and Aβ-mediated cytotoxicity and reduce the levels of Aβ in the brain and increase Aβ clearance.