| Summary: | 碩士 === 國立臺灣師範大學 === 生命科學研究所 === 98 === Alzheimer’s disease (AD) is a progressive neurodegenerative disease affecting the elderly population. Two primary features were characterized for the disease, plaques composed of aggregate amyloid-beta (Aβ) and neurofibrillary tangles (NFT) consisting of hyperphosphorylated tau protein. These neuropathologies are closely linked with chronic inflammation, oxidative stress and neurotransmitter dysregulation. Many evidences show that exercise is beneficial to the brain and cognitive function through multiple pathways. Therefore, the present studies conducted moderate, no shock treadmill running exercise on aged (21~ 24 months) and young (7~ 8 months) APP/PS1 transgenic and littermate male mice for four weeks. Age matched sedentary groups were also included in this study. Exercise enhanced exploratory behavior in young APP/PS1 transgenic mice and decreased the level of the serum corticosterone. In addition, moderate exercise improved only the spatial reference learning and memory, not spatial working memory or exploratory behavior in aged APP/PS1 transgenic mice. The results from pathologic analysis show exercise decreased the level of the insoluble Aβ42/Aβ40 ratio in young APP/PS1 transgenic mice. Exercise increased the blood glucose (BG) level in aged APP/PS1 transgenic mice. Furthermore, exercise also increased the level of the serotonergic immunoreactive neurons in the APP/PS1 transgenic mice. In summary, we found that moderate, non-shock treadmill exercise can selective improve behavior, cognitive performance and the pathogenic phenotypes in the APP/PS1 transgenic mice.
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