Effect of Vitamin E on Learning and Memory Deficit in Aged Rats

Abstract

Summary In order to verify whether vitamin E improves the cognitive impairment induced through aging, aged rats fed a vitamin E-supplemented diet had their learning and memory functions assessed in comparison with the aged rats fed a normal diet using a Morris water maze test. Although normal aged rats showed very poor learning ability concerning the place of a platform in the water maze apparatus, the aged rats fed the vitamin Esupplemented diet learned the place with a marked speed in only 5 trials. After old animals showed the maximum learning ability, they were kept in a normal atmosphere for 48 h without a trial followed by an assessment of their memory function using the same apparatus. The vitamin E-supplementation to aged rats resulted in marked retention of their maximum memory function, although normal aged rats showed a significant memory loss of about 60%. Pyrroloquinoline quinone (PQQ), which increases in the production of nerve growth factor, and protects neurons, had a similar effect on cognitive function to that of vitamin E in the aged rats. These results suggest that vitamin E may improve cognitive deficit caused through aging by not only its neuro-protecting effect but an antioxidant efficacy. Key Words vitamin E, cognitive deficit, learning, memory, aged rat Although it has been recognized that normal aging is accompanied by declines in cognitive performance, the precise mechanisms leading to this deficit during aging are not well understood. It is evident that these declines arise from neurodegeneration through several factors during aging such as stroke, cerebral infarction and oxidative stress. There is substantial notion that oxidative stress is relevant to the aging process. Oxidative stress occurs at the time of an imbalance between reactive oxygen species (ROS) generation and its detoxification by antioxidants in living tissues, so that aging is considered to be accumulation of oxidative damage of living tissues through oxidative stress experienced over a long period of time ( 1 , 2 ).Among organs in living tissues, neurons in the brain are considered to be more vulnerable to oxidative stress than other organs, leading to neuronal oxidative damage, and neurodegenerative disorders such as Alzheimer's disease (AD), Parkinsonism and senile dementia ( 3 ). It is well-characterized that there are increased regional levels of oxidative stress in the AD brain, and hence recent studies have demonstrated a decrease in polyunsaturated fatty acids, increased levels of lipid peroxidation markers, protein oxidation, and DNA and RNA oxidation in AD ( 4 ). Based on the oxidative stress theory of brain aging, our previous study revealed that the levels of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides, F 2 -isoprostane and conjugated dienes increase significantly with oxidative stress in the rat brain, and the activity of antioxidative enzymes and vitamin E content in the brain decrease markedly ( 5-7 ). Furthermore, in accordance with these phenomena, young rats subjected to ox...

Recent progress in studies on the health benefits of pyrroloquinoline quinone

“…Similar effects were observed in aged rats. 86) These results suggest that PQQ is potentially effective for preventing neurodegeneration caused by oxidative stress.…”

α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions

“…In old rats chronically fed α-T supplemented diet, age-related increases in interleukin-1β and lipid peroxidation were reversed, and the concurrent improvement of LTP in the dentate gyrus (DG) was linearly correlated with brain α-T levels [39]. In keeping, behavioral studies have shown that aged rats supplemented with vitamin E exhibit improved learning speed and retention memory on hippocampus-dependent spatial cognitive tasks (Morris water maze) in comparison with age-matched rats fed a normal diet [131]. Moreover, supplementing rats with a combination of N -acetylcysteine, α-lipoic acid and α-T, was able to prevent age-dependent alterations in brain synaptosomal parameters (i.e., increased membrane potential with altered content of Na + and K + under both basal and stimulated conditions) and the impairment in learning and memory functions examined on T-maze [132].…”

Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication

“…Therefore, the numbers of neurons in this part were estimated to evaluate the effect of 1-BP on the survival of neurons in Hippocampus. It has been reported that the impairment of memory ability and spatial learning could be resulted from loss of neuron, 27 we next examined the status of neuron loss in each group. The brains were harvested, sectioned, and stained with Neun to count the neurons in each group.…”