The purpose of this study was to determine if relatively short-term vitamin E supplementation could reverse age-associated impairments in cognitive or motor function and the accumulated oxidative damage in the brain of aged mice. Separate groups of 5- or 20-month-old C57BL6 mice were placed on either a control diet or the same diet supplemented with α-tocopheryl acetate (1.65 g/kg). After 4 weeks on the diets, mice were tested for cognitive and motor functions over the next 8 weeks, during which the supplementation was maintained. Vitamin E supplementation increased the concentration of α-tocopherol in the cerebral cortex of both the young and old mice, but did not significantly affect oxidative damage to proteins and lipids in the brain cortex. When compared with young controls, the old control mice showed slower learning of a swim maze, longer reaction times, diminished auditory and shock-startle responsiveness, and diminished motor performance on tests of coordinated running and bridge walking. The vitamin E-administered old mice failed to show improvement of function relative to age-matched controls on any of the tests, but did show altered retention performance on the swim maze task and impaired performance in the test of coordinated running. The latter effects were not evident in young mice on the supplemented diet. Results of this study suggest that, when implemented in relatively old mice, supplementation of vitamin E is ineffective in reversing preexisting age-related impairments of cognitive or motor function, and has little effect on common measures of protein or lipid oxidative damage in the mouse brain. Moreover, the current findings indicate that vitamin E could have detrimental effects on some brain functions when implemented in older animals.