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Neurobiol Aging. 2015 Nov;36(11):2984-2994. doi: 10.1016/j.neurobiolaging.2015.07.022. Epub 2015 Jul 18.

Impaired cognition and cerebral glucose regulation are associated with astrocyte activation in the parenchyma of metabolically stressed APPswe/PS1dE9 mice.

Author information

1
Institute of Neuroscience, Brain Research Center, School of Life Science, National Yang-Ming University, Taipei, Taiwan, Republic of China.
2
Brain Research Center, National Yang Ming University, Taipei, Taiwan, Republic of China; Biophotonic and Molecular Imaging Research Center, National Yang Ming University, Taipei, Taiwan, Republic of China.
3
Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli County, Taiwan, Republic of China.
4
Department of Psychology, Graduate Institute of Brain and Mind Sciences, Neurobiology and Cognitive Science Center, National Taiwan University, Taipei, Taiwan, Republic of China.
5
Division of Basic Chinese Medicine, National Research Institute of Chinese Medicine, Taipei, Taiwan, Republic of China; Ph.D. Program for the Clinical Drug Discovery from Botanical Herbs, Taipei Medical University, Taiwan, Republic of China.
6
Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei, Taiwan, Republic of China.
7
Institute of Neuroscience, Brain Research Center, School of Life Science, National Yang-Ming University, Taipei, Taiwan, Republic of China. Electronic address: hjtsay@ym.edu.tw.
8
Division of Basic Chinese Medicine, National Research Institute of Chinese Medicine, Taipei, Taiwan, Republic of China; Ph.D. Program for the Clinical Drug Discovery from Botanical Herbs, Taipei Medical University, Taiwan, Republic of China; Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei, Taiwan, Republic of China. Electronic address: yshiao@nricm.edu.tw.

Abstract

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 [(18)F]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.

KEYWORDS:

Alzheimer's disease; Amyloid plaque; Astrocytes; Cerebral glucose regulation; Cognitive dysfunction; Metabolic stresses

[Indexed for MEDLINE]

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