Vitamin E supplementation prevents spatial learning deficits and dendriticalterations in aged apolipoprotein E-deficient mice

Recent studies have suggested that altered function of apolipoprotein E mig ht lead to Alzheimer's disease via oxidative stress. In this context, the o bjective of this study was to determine if antioxidative treatment with vit amin E was neuroprotective in apolipoprotein E-deficient mice. For this pur pose, 1-month-old control and apolipoprotein E-deficient mice received diet ary vitamin E for 12 months. We showed that, compared to apolipoprotein E-d eficient mice who received a regular diet, mice treated with vitamin E disp layed a significantly improved behavioural performance in the Morris water maze. This improved performance was associated with preservation of the den dritic structure in vitamin E-treated apolipoprotein E-deficient mice. In a ddition, whilst untreated apolipoprotein E-deficient mice displayed increas ed levels of lipid peroxidation and glutathione, vitamin E-treated mice sho wed near normal levels of both lipid peroxidation and glutathione. These re sults support the contention that vitamin E prevents the age-related neurod egenerative alterations in apolipoprotein E-deficient mice.