https://scholars.lib.ntu.edu.tw/handle/123456789/509844
標題: | Impaired cognition and cerebral glucose regulation are associated with astrocyte activation in the parenchyma of metabolically stressed APPswe/PS1dE9 mice | 作者: | Yeh, C.-W. Yeh, S.H.-H. Shie, F.-S. Lai, W.-S. Liu, H.-K. Tzeng, T.-T. Tsay, H.-J. WEN-SUNG LAI |
公開日期: | 2015 | 卷: | 36 | 期: | 11 | 起(迄)頁: | 2984-2994 | 來源出版物: | Neurobiology of Aging | 摘要: | Although metabolic syndrome was suggested to be a risk factor for Alzheimer's disease (AD), the role of metabolic stress in the initiation of AD pathology remains unclear. In this study, metabolic stress was induced by a high-fat diet and low-dose injection of streptozotocin (HFSTZ) before the appearance of senile plaques in APP/PS1 transgenic mice. We found that, HFSTZ treatment exacerbated amyloid beta burden and astrocyte activation in the vicinity of plaques. Moreover, we observed an upregulation of astrocytic S100B expression in the brain parenchyma of HFSTZ-treated APP/PS1 mice concurrent with increased interleukin-6 expression in cerebral microvascular cells. To determine the impact of HFSTZ treatment on brain function, we performed [18F]fludeoxyglucose-positron emission tomography and analyzed nesting behavior. HFSTZ treatment impaired nest construction and cerebral glucose metabolism in several brain regions of APP/PS1 mice during the early stage of AD. These results suggest that HFSTZ-induced peripheral metabolic stress may contribute to vascular inflammation and astrocyte reactivity in the parenchyma and may impair activity of daily living skill and cerebral glucose metabolism in APP/PS1 mice. ? 2015 Elsevier Inc. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/509844 | DOI: | 10.1016/j.neurobiolaging.2015.07.022 | SDG/關鍵字: | amyloid beta protein[1-40]; amyloid beta protein[1-42]; glial fibrillary acidic protein; interleukin 6; protein S100B; amyloid beta protein; glial fibrillary acidic protein; glial fibrillary astrocytic protein, mouse; glucose; interleukin 6; protein S100B; S100b protein, mouse; streptozocin; Alzheimer disease; animal experiment; animal model; animal tissue; Article; astrocyte; cell activation; cognitive defect; controlled study; disease association; female; glucose metabolism; hyperglycemia; male; mouse; nesting; neuropathology; nonhuman; obesity; priority journal; protein expression; spatial learning; spatial memory; upregulation; Alzheimer disease; amyloid plaque; animal; brain; Cognition Disorders; metabolic syndrome X; metabolism; microvasculature; obesity; pathology; physiological stress; physiology; transgenic mouse; vascularization; Alzheimer Disease; Amyloid beta-Peptides; Animals; Astrocytes; Brain; Cognition Disorders; Glial Fibrillary Acidic Protein; Glucose; Interleukin-6; Male; Metabolic Syndrome X; Mice, Transgenic; Microvessels; Obesity; Plaque, Amyloid; S100 Calcium Binding Protein beta Subunit; Streptozocin; Stress, Physiological |
顯示於: | 心理學系 |
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