Imaging of amyloid β in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer:: proof of mechanism

Imaging of amyloid β in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer:: proof of mechanism
复制标题

DOI:
10.1016/s1474-4422(08)70001-2
复制
发表时间:
2008-02-01
期刊:
影响因子:
48
通讯作者:
Villemagne, Victor L.
Villemagne, Victor L.
中科院分区:
医学1区
文献类型:
--
作者:
Rowe, Christopher C.;Ackerman, Uwe;Villemagne, Victor L.

文献摘要

被引文献

相似文献

淀粉样β蛋白(AP)斑块的形成是阿尔茨海默病(AD)的标志,并先于痴呆的发作。β成像应该允许早期诊断,但临床应用受到当前β特异性配体的短衰变半衰期的阻碍。F-18-BAY 94 -9172是一种A β配体,由于F-18的半衰期,适合临床使用。因此,我们研究了这种配体在识别AD患者的有效性。方法15例轻度AD患者,15名健康老年人对照,和5个人额颞叶变性(FTLD)进行了研究。通过使用标准化摄取值比率(SUVR)定量F-18-BAY 94 -9172结合,该比率通过使用小脑作为参考区域计算新皮质。SUVR图像视觉评定为正常或AD。F-18-BAY 94 -9172结合结果与报告的A β斑块死后分布相匹配。所有AD患者表现出广泛的新皮质结合,这是更大的楔前叶/后扣带和额叶皮质比外侧颞叶和顶叶皮质。感觉运动、枕叶和内侧颞叶皮质相对较少。健康对照组和FTLD患者仅显示白质结合,尽管三名对照组和一名FTLD患者在额叶和前额皮质有轻度摄取。在注射后90-120分钟,AD患者的新皮层SUVR(2.0 [SD 0-3])高于健康对照组(1-3 [SD 0 - 21; p
Background Amyloid-beta (AP) plaque formation is a hallmark of Alzheimer's disease (AD) and precedes the onset of dementia. A beta imaging should allow earlier diagnosis, but clinical application is hindered by the short decay half-life of current A beta-specific ligands. F-18-BAY94-9172 is an A beta ligand that, due to the half-life of F-18, 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. F-18-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 F-18-BAY94-9172 binding matched the reported post-mortem distribution of A beta 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 prectineus 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 - 21; p