Abha Chauhan and Ved Chauhan
Amyloid beta-protein (Aβ) is that the major protein of amyloid deposits within the brain of patients with Alzheimer’s disease (AD). Extensive evidence suggests neurotoxic effects of Aβ and also 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 necrobiosis in PC12 cells. within the Tg2576 transgenic mouse model of AD (AD-tg), we've 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 put next to AD-Tg mice on diet without walnuts (T0). The diets for the experimental and control mice were comparable as regards total calories and therefore the contents of protein, carbohydrate and fat. To understand the mechanism of beneficial effects of diet with walnuts in AD, we've recently studied the consequences of walnuts on Aβ levels and oxidative stress markers in AD mice. In AD-tg mice on diet with walnuts (T6, T9), the degree of soluble Aβ was lower within the brain and better within the blood in comparison to T0 mice, suggesting that walnuts within the diet can increase the clearance of Aβ from the brain to the blood. We also observed a significant decrease in atom levels and oxidative damage (lipid peroxidation, protein oxidation) as well as increased antioxidant status (superoxide dismutase, catalase, and glutathione peroxidase) in these T6 and T9 mice on diet with walnuts. last, these studies suggest that diet with walnuts may have beneficial effects in reducing the chance, delaying the onset, or slowing the progression of AD because walnuts can help to boost memory and learning skills, inhibit Aβ fibrillization and maintain Aββ within the soluble form, decrease Aβinduced oxidative stress and Aβ-mediated cytotoxicity and reduce the degree of Aβ within the brain and increase Aβ clearance.
