Browsing by Subject "vitamin E"
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Item ApoE Genotype-Dependent Response to Antioxidant and Exercise Interventions on Brain Function(MDPI, 2020-06-25) Chaudhari, Kiran; Wong, Jessica M.; Vann, Philip H.; Como, Tori; O'Bryant, Sid E.; Sumien, NathalieThis study determined whether antioxidant supplementation is a viable complement to exercise regimens in improving cognitive and motor performance in a mouse model of Alzheimer's disease risk. Starting at 12 months of age, separate groups of male and female mice expressing human Apolipoprotein E3 (GFAP-ApoE3) or E4 (GFAP-ApoE4) were fed either a control diet or a diet supplemented with vitamins E and C. The mice were further separated into a sedentary group or a group that followed a daily exercise regimen. After 8 weeks on the treatments, the mice were administered a battery of functional tests including tests to measure reflex and motor, cognitive, and affective function while remaining on their treatment. Subsequently, plasma inflammatory markers and catalase activity in brain regions were measured. Overall, the GFAP-ApoE4 mice exhibited poorer motor function and spatial learning and memory. The treatments improved balance, learning, and cognitive flexibility in the GFAP-ApoE3 mice and overall the GFAP-ApoE4 mice were not responsive. The addition of antioxidants to supplement a training regimen only provided further benefits to the active avoidance task, and there was no antagonistic interaction between the two interventions. These outcomes are indicative that there is a window of opportunity for treatment and that genotype plays an important role in response to interventions.Item Lifelong vs. Late Life Tocopherol on Learning and Memory in Mice(2004-05-01) McDonald, Shelley R.; Michael Forster; Glenn DillonMcDonald, Shelley R., Lifelong vs. late life tocopherol on learning and memory in mice. Doctor of Philosophy (Biomedical Sciences), May, 2004, 132 pp., 1 table, 14 figures, bibliography, 122 titles. The purpose of these studies was to determine if vitamin E supplementation, a well-studied antioxidant, could improve the cognitive functions of old mice either by preventing age-dependent impairments or reversing age-related dysfunction. Cellular oxidative stress is believed to be a causal factor in senescence, and the brain appears to be particularly susceptible to oxidative damage because of a relatively high rate of reactive oxygen species generation without commensurate levels of antioxidant defenses. If oxidative stress indeed plays a role in age-related brain dysfunction, then it can be predicted that experimental interventions capable of lowering oxidative stress would either prevent or restore function. This was tested using apolipoprotein E-deficient mice, which have an increased susceptibility to neuronal oxidative damage, maintained on 3 different doses (2 mg/kg, 20 mg/kg, or 200 mg/kg/day) of dl-α-tocopheryl acetate (vitamin E) via supplemented food pellets from 8 weeks of age throughout behavioral testing when 6 or 18 mo of age. A separate experiment used wild type mice 24 months of age to examine whether or not a combination of vitamin E (123 mg/kg/day) with coenzyme Q10 (200 mg/kg/day) which leads to higher tissue levels of vitamin E, could improve brain functions in old mice. Mice were tested on multiple behavioral tasks that required utilization of various components of memory and learning, as well as sensorimotor testing. The highest dose of vitamin E prevented the decline of spatial memory in old apolipoprotein E-deficient mice, but did not prevent age-related impairments in learning and memory for discriminated escape. When old wild type mice were treated with the combined vitamin E and coenzyme W10, the mice learned and remembered to avoid a preemptive shock significantly more than old mice treated with vitamin E or coenzyme Q10 alone. A followup experiment with higher doses of coenzyme Q10 alone (250 or 500 mg/kg/day) resulted in no cognitive improvements. No treatments improved sensorimotor performance.