European Institute for Molecular Imaging, Westfalian Wilhelms-University Münster, Münster, Germany.
Neurobiol Aging. 2013 Jan;34(1):351-4. doi: 10.1016/j.neurobiolaging.2012.04.016. Epub 2012 May 30.
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 [(11)C]-(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). [(11)C]-(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, [(11)C]-(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.
在阿尔茨海默病（AD）中，持续性小胶质细胞激活作为慢性神经炎症的标志，导致疾病进展。我们的研究旨在通过正电子发射断层扫描（PET）使用[（11）C] - （R） - PK11195对 13 至 15 个月大的 AD 小鼠体内可视化和量化小胶质细胞激活。我们试图通过用吡格列酮（5 周治疗，5 周洗脱期）对动物进行抗炎治疗来调节神经炎症。在 15 个月洗脱期后，AD 小鼠的[（11）C] - （R） - PK11195分布容积值明显高于对照组小鼠，这得到免疫组织化学数据的支持。然而，[（11）C] - （R） - PK11195 μPET 不能在 13 至 14 个月大的动物中显示基因型或治疗依赖性差异，表明在该年龄和疾病阶段 AD 小鼠的小胶质细胞激活太轻微，无法通过这种成像方法检测到。
