11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration

11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration
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DOI:
10.1212/01.wnl.0000259035.98480.ed
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发表时间:
2007-04-10
期刊:
影响因子:
9.9
通讯作者:
Jagust, W. J.
Jagust, W. J.
中科院分区:
医学1区
文献类型:
--
作者:
Rabinovici, G. D.;Furst, A. J.;Jagust, W. J.

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背景资料:PET示踪剂C-11标记的匹兹堡化合物-B(C-11-PIB)特异性结合纤维状淀粉样蛋白-β(A β)斑块,并且可以在阿尔茨海默病(AD)中检测到。我们假设,PET成像与C-11-PIB将区分AD额颞叶变性(FTLD),非A β痴呆。研究方法:符合AD(n = 7)或FTLD(n = 12)研究标准的患者和认知正常对照(n = 8)接受了C-11-PIB(患者和对照)和F-18-氟脱氧葡萄糖(F-18-FDG)(仅患者)PET成像。C-11-PIB全脑和感兴趣区域(ROI)分布体积比(DVR)采用Logan图形分析计算,小脑作为参考区域。DVR图像由设盲的研究者视觉评定为皮质C-11-PIB阳性或阴性,F-18-FDG图像总和评定为与AD或FTLD一致。结果如下:所有AD患者(7/7)目视检查C-11-PIB扫描均为阳性,而8/12例FTLD患者和7/8例对照组均为阴性。在4例PIB阳性FTLD患者中,2例F-18-FDG扫描提示AD,2例F-18-FDG扫描提示FTLD。AD患者的全脑、外侧额叶、楔前叶和外侧颞叶皮质的平均DVR高于FTLD患者(p < 0.05),而FTLD患者的DVR与对照组无显著差异。结论:用C-11标记的匹兹堡化合物-B(C-11-PIB)进行PET成像有助于区分阿尔茨海默病(AD)和额颞叶变性(FTLD)。需要病理相关性来确定PIB阳性FTLD患者是否代表假阳性、FTLD/AD共病病理或模拟FTLD临床综合征的AD病理。
Background: The PET tracer C-11-labeled Pittsburgh Compound-B (C-11-PIB) specifically binds fibrillar amyloid-beta (A beta) plaques and can be detected in Alzheimer disease (AD). We hypothesized that PET imaging with C-11-PIB would discriminate AD from frontotemporal lobar degeneration (FTLD), a non-A beta dementia. Methods: Patients meeting research criteria for AD (n = 7) or FTLD (n = 12) and cognitively normal controls (n = 8) underwent PET imaging with C-11-PIB (patients and controls) and F-18-fluorodeoxyglucose (F-18-FDG) (patients only). C-11-PIB whole brain and region of interest (ROI) distribution volume ratios (DVR) were calculated using Logan graphical analysis with cerebellum as a reference region. DVR images were visually rated by a blinded investigator as positive or negative for cortical C-11-PIB, and summed F-18-FDG images were rated as consistent with AD or FTLD. Results: All patients with AD (7/7) had positive C-11-PIB scans by visual inspection, while 8/12 patients with FTLD and 7/8 controls had negative scans. Of the four PIB-positive patients with FTLD, two had F-18-FDG scans that suggested AD, and two had F-18-FDG scans suggestive of FTLD. Mean DVRs were higher in AD than in FTLD in whole brain, lateral frontal, precuneus, and lateral temporal cortex (p < 0.05), while DVRs in FTLD did not significantly differ from controls. Conclusions: PET imaging with C-11-labeled Pittsburgh Compound-B (C-11-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD). Pathologic correlation is needed to determine whether patients with PIB-positive FTLD represent false positives, comorbid FTLD/AD pathology, or AD pathology mimicking an FTLD clinical syndrome.