PDF(Pubmed)
Abstract：
Emerging evidence suggests a potential causal role of neuroinflammation in Alzheimer\'s disease (AD). Using positron emission tomography (PET) to image overexpressed 18 kDA translocator protein (TSPO) by activated microglia has gained increasing interest. The uptake of 18F-GE180 TSPO PET was observed to co-localize with inflammatory markers and have a two-stage association with amyloid PET in mice. Very few studies evaluated the diagnostic power of 18F-GE180 PET in AD population and its interpretation in human remains controversial about whether it is a marker of microglial activation or merely reflects disrupted blood-brain barrier integrity in humans.
The goal of this study was to study human GE180 from the perspective of the previous animal observations.
With data from twenty-four participants having 18F-GE180 and 18F-AV45 PET scans, we evaluated the group differences of 18F-GE180 uptake between participants with and without cognitive impairment. An association analysis of 18F-GE180 and 18F-AV45 was then conducted to test if the relationship in humans is consistent with the two-stage association in AD mouse model.
Elevated 18F-GE180 was observed in participants with cognitive impairment compared to those with normal cognition. No regions showed reduced 18F-GE180 uptake. Consistent with mouse model, a two-stage association between 18F-GE180 and 18F-AV45 was observed.
18F-GE180 PET imaging showed promising utility in detecting pathological alterations in a symptomatic AD population. Consistent two-stage association between 18F-GE180 and amyloid PET in human and mouse suggested that 18F-GE180 uptake in human might be considerably influenced by microglial activation.
The goal of this study was to study human GE180 from the perspective of the previous animal observations.
With data from twenty-four participants having 18F-GE180 and 18F-AV45 PET scans, we evaluated the group differences of 18F-GE180 uptake between participants with and without cognitive impairment. An association analysis of 18F-GE180 and 18F-AV45 was then conducted to test if the relationship in humans is consistent with the two-stage association in AD mouse model.
Elevated 18F-GE180 was observed in participants with cognitive impairment compared to those with normal cognition. No regions showed reduced 18F-GE180 uptake. Consistent with mouse model, a two-stage association between 18F-GE180 and 18F-AV45 was observed.
18F-GE180 PET imaging showed promising utility in detecting pathological alterations in a symptomatic AD population. Consistent two-stage association between 18F-GE180 and amyloid PET in human and mouse suggested that 18F-GE180 uptake in human might be considerably influenced by microglial activation.
摘要：
背景：新的证据表明神经炎症在阿尔茨海默病（AD）中具有潜在的因果作用。使用正电子发射断层扫描（PET）对激活的小胶质细胞过度表达的18kDA转运蛋白（TSPO）进行成像已引起越来越多的兴趣。观察到18F-GE180TSPOPET的摄取与炎症标志物共定位，并与小鼠的淀粉样蛋白PET具有两阶段关联。很少有研究评估18F-GE180PET在AD人群中的诊断能力，其在人类中的解释仍然存在争议，因为它是小胶质细胞激活的标志物还是仅仅反映了人类血脑屏障完整性的破坏。
目的：本研究的目的是从先前动物观察的角度研究人类GE180。
方法：根据24名接受18F-GE180和18F-AV45PET扫描的参与者的数据，我们评估了有和无认知障碍参与者18F-GE180摄取的组间差异.然后进行18F-GE180和18F-AV45的关联分析以测试人类中的关系是否与AD小鼠模型中的两阶段关联一致。
结果：与认知正常的参与者相比，在认知障碍的参与者中观察到18F-GE180升高。没有区域显示18F-GE180摄取减少。与小鼠模型一致，观察到18F-GE180和18F-AV45之间存在两阶段关联.
结论：18F-GE180PET显像在检测有症状的AD人群的病理改变方面显示出很有希望的应用。在人和小鼠中18F-GE180和淀粉样蛋白PET之间的一致的两阶段关联表明，人的18F-GE180摄取可能受到小胶质细胞激活的很大影响。
目的：本研究的目的是从先前动物观察的角度研究人类GE180。
方法：根据24名接受18F-GE180和18F-AV45PET扫描的参与者的数据，我们评估了有和无认知障碍参与者18F-GE180摄取的组间差异.然后进行18F-GE180和18F-AV45的关联分析以测试人类中的关系是否与AD小鼠模型中的两阶段关联一致。
结果：与认知正常的参与者相比，在认知障碍的参与者中观察到18F-GE180升高。没有区域显示18F-GE180摄取减少。与小鼠模型一致，观察到18F-GE180和18F-AV45之间存在两阶段关联.
结论：18F-GE180PET显像在检测有症状的AD人群的病理改变方面显示出很有希望的应用。在人和小鼠中18F-GE180和淀粉样蛋白PET之间的一致的两阶段关联表明，人的18F-GE180摄取可能受到小胶质细胞激活的很大影响。
