Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease |
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Authors: | Sara Rapic Heiko Backes Thomas Viel Markus P Kummer Parisa Monfared Bernd Neumaier Stefan Vollmar Mathias Hoehn Annemie Van der Linden Michael T Heneka Andreas H Jacobs |
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Institution: | 1. European Institute for Molecular Imaging (EIMI), Westfalian Wilhelms-University (WWU) Münster, Münster, Germany;2. Interdisciplinary Centre for Clinical Research (IZKF), WWU Münster, Münster, Germany;3. Max Planck Institute for Neurological Research, Cologne, Germany;4. Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany;5. Bio-Imaging Lab, University of Antwerp, Antwerp, Belgium;6. Department of Nuclear Medicine, WWU Münster, Münster, Germany |
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Abstract: | In Alzheimer's disease (AD), persistent microglial activation as sign of chronic neuroinflammation contributes to disease progression. Our study aimed to in vivo visualize and quantify microglial activation in 13- to 15-month-old AD mice using 11C]-(R)-PK11195 and positron emission tomography (PET). We attempted to modulate neuroinflammation by subjecting the animals to an anti-inflammatory treatment with pioglitazone (5-weeks' treatment, 5-week wash-out period). 11C]-(R)-PK11195 distribution volume values in AD mice were significantly higher compared with control mice after the wash-out period at 15 months, which was supported by immunohistochemistry data. However, 11C]-(R)-PK11195 μPET could not demonstrate genotype- or treatment-dependent differences in the 13- to 14-month-old animals, suggesting that microglial activation in AD mice at this age and disease stage is too mild to be detected by this imaging method. |
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Keywords: | Alzheimer's disease Inflammation Microglia Molecular imaging Positron emission tomography PK11195 PPAR-gamma Transgenic mice |
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