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首页> 外文期刊>Lancet Neurology >Imaging of amyloid beta in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism.
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Imaging of amyloid beta in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism.

机译：使用新型PET示踪剂18F-BAY94-9172对阿尔茨海默氏病中的淀粉样蛋白β进行成像：机制的证明。

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BACKGROUND: Amyloid-beta (Abeta) plaque formation is a hallmark of Alzheimer's disease (AD) and precedes the onset of dementia. Abeta imaging should allow earlier diagnosis, but clinical application is hindered by the short decay half-life of current Abeta-specific ligands. (18)F-BAY94-9172 is an Abeta ligand that, due to the half-life of (18)F, is suitable for clinical use. We thus studied the effectiveness of this ligand in identifying patients with AD. METHODS: 15 patients with mild AD, 15 healthy elderly controls, and five individuals with frontotemporal lobar degeneration (FTLD) were studied. (18)F-BAY94-9172 binding was quantified by use of the standardised uptake value ratio (SUVR), which was calculated for the neocortex by use of the cerebellum as reference region. SUVR images were visually rated as normal or AD. FINDINGS: (18)F-BAY94-9172 binding matched the reported post-mortem distribution of Abeta plaques. All AD patients showed widespread neocortical binding, which was greater in the precuneus/posterior cingulate and frontal cortex than in the lateral temporal and parietal cortex. There was relative sparing of sensorimotor, occipital, and medial temporal cortex. Healthy controls and FTLD patients showed only white-matter binding, although three controls and one FTLD patient had mild uptake in frontal and precuneus cortex. At 90-120 min after injection, higher neocortical SUVR was observed in AD patients (2.0 [SD 0.3]) than in healthy controls (1.3 [SD 0.2]; p<0.0001) or FTLD patients (1.2 [SD 0.2]; p=0.009). Visual interpretation was 100% sensitive and 90% specific for detection of AD. INTERPRETATION: (18)F-BAY94-9172 PET discriminates between AD and FTLD or healthy controls and might facilitate integration of Abeta imaging into clinical practice.
机译：背景：淀粉样蛋白（Abeta）斑块的形成是阿尔茨海默氏病（AD）的标志，并且早于痴呆。 Abeta成像应允许早期诊断，但是当前Abeta特异性配体的衰变半衰期短，临床应用受到了阻碍。 （18）F-BAY94-9172是一种Abeta配体，由于（18）F的半衰期而适合临床使用。因此，我们研究了该配体在识别AD患者中的有效性。方法：研究了15例轻度AD患者，15例健康的老年对照和5例额颞叶变性（FTLD）患者。 （18）F-BAY94-9172的结合是通过使用标准化摄取值比（SUVR）来定量的，所述SUVR是通过以小脑作为参考区域来计算新皮质的。 SUVR图像在视觉上被评为正常或AD。结果：（18）F-BAY94-9172绑定匹配报告的Abeta斑的验尸分布。所有AD患者均表现出广泛的新皮质结合，在前皮/后扣带和额皮质中比在颞外侧和顶叶皮质中更大。感觉运动，枕叶和颞内侧皮质相对较少。健康的对照组和FTLD患者仅表现出白质结合，尽管三名对照组和一名FTLD患者的额叶皮层和早孕皮层有轻度摄取。注射后90-120分钟，AD患者（2.0 [SD 0.3]）观察到的新皮层SUVR高于健康对照组（1.3 [SD 0.2]; p <0.0001）或FTLD患者（1.2 [SD 0.2]; p = 0.009）。视觉解释对AD的检测具有100％的敏感性和90％的特异性。解释：（18）F-BAY94-9172 PET区分AD和FTLD或健康对照，可能有助于将Abeta成像整合到临床实践中。

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