Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease

被引:40
作者
Rapic, Sara [1 ,2 ,3 ]
Backes, Heiko [3 ]
Viel, Thomas [1 ,3 ]
Kummer, Markus P. [4 ]
Monfared, Parisa [1 ,3 ]
Neumaier, Bernd [3 ]
Vollmar, Stefan [3 ]
Hoehn, Mathias [3 ]
Van der Linden, Annemie [5 ]
Heneka, Michael T. [4 ]
Jacobs, Andreas H. [1 ,2 ,6 ]
机构
[1] Westfal Wilhelms Univ Munster WWU, EIMI, D-48149 Munster, Germany
[2] WWU Munster, Interdisciplinary Ctr Clin Res IZKF, Munster, Germany
[3] Max Planck Inst Neurol Res, D-50931 Cologne, Germany
[4] Univ Bonn, Dept Neurol, Bonn, Germany
[5] Univ Antwerp, Bioimaging Lab, B-2020 Antwerp, Belgium
[6] WWU Munster, Dept Nucl Med, Munster, Germany
关键词
Alzheimer's disease; Inflammation; Microglia; Molecular imaging; Positron emission tomography; PK11195; PPAR-gamma; Transgenic mice;
D O I
10.1016/j.neurobiolaging.2012.04.016
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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 [C-11]-(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). [C-11]-(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, [C-11]-(R)-PK11195 mu PET 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. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:351 / 354
页数:4
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