Use of florbetapir-PET for imaging beta-amyloid pathology.

Use of florbetapir-PET for imaging beta-amyloid pathology.
复制标题

DOI:
10.1001/jama.2010.2008
复制
发表时间:
2011-01-19
期刊:
JAMA
影响因子:
--
通讯作者:
AV45-A07 Study Group
AV45-A07 Study Group
中科院分区:
其他
文献类型:
--
作者:
Clark CM;Schneider JA;Bedell BJ;Beach TG;Bilker WB;Mintun MA;Pontecorvo MJ;Hefti F;Carpenter AP;Flitter ML;Krautkramer MJ;Kung HF;Coleman RE;Doraiswamy PM;Fleisher AS;Sabbagh MN;Sadowsky CH;Reiman EP;Zehntner SP;Skovronsky DM;AV45-A07 Study Group

文献摘要

参考文献

被引文献

相似文献

识别和定量脑β-淀粉样蛋白的能力可以提高阿尔茨海默病临床诊断的准确性。确定在生前进行的florbetapir F 18正电子发射断层扫描(PET)成像是否能准确预测尸检时大脑中β-淀粉样蛋白的存在。2009年2月至2010年3月对临终关怀、长期护理和社区医疗机构的35例患者(6例患者建立方案,29例患者验证)进行的florbetapir-PET成像进行了前瞻性临床评价,并将其死亡后脑β-淀粉样蛋白的免疫组织化学和银染色测量作为参考标准进行了比较。还对74名假定无脑淀粉样蛋白的年轻人(18-50岁)进行了PET图像,以更好地了解氟倍他普利-PET图像假阳性解读的频率。在前35例尸检参与者(入组PET病理相关性研究的152例个体中)中,florbetapir-PET图像解读(基于3名核医学医师评分的中位数)和皮质滞留的半自动定量与死后β-淀粉样蛋白负荷、神经炎性淀粉样蛋白斑块密度和阿尔茨海默病的神经病理学诊断的相关性。主要分析队列中的29名个体在死亡前平均99天(范围,1-377天)进行了Florbetapir-PET成像。29人中有15人(51.7%)符合阿尔茨海默病的病理标准。通过免疫组织化学检测,在尸检时,florbetapir-PET图像的视觉判读和皮质摄取的平均定量估计值与β淀粉样蛋白病理学的存在和数量相关(Bonferroni ρ,0.78 [95%置信区间,0.58-0.89]; P<.001])和银染色神经炎斑块评分(Bonferroni ρ,0.71 [95%可信区间,0.47-0.86]; P<.001)。在主要分析队列的29名个体中,96%的人的Florbetapir-PET图像和尸检结果被评定为β-淀粉样蛋白阳性或阴性。在非尸检队列中,74名年轻个体的florbetapir-PET图像被评定为淀粉样蛋白阴性。Florbetapir-PET成像与β-淀粉样蛋白的存在和密度相关。这些数据提供了证据,表明分子成像程序可以识别个体在生命期间大脑中的β-淀粉样蛋白病理学。需要进行更多的研究,以了解在阿尔茨海默病的临床诊断和预测进展为痴呆症的适当使用florbetapir-PET成像。
The ability to identify and quantify brain β-amyloid could increase the accuracy of a clinical diagnosis of Alzheimer disease. To determine if florbetapir F 18 positron emission tomographic (PET) imaging performed during life accurately predicts the presence of β-amyloid in the brain at autopsy. Prospective clinical evaluation conducted February 2009 through March 2010 of florbetapir-PET imaging performed on 35 patients from hospice, long-term care, and community health care facilities near the end of their lives (6 patients to establish the protocol and 29 to validate) compared with immunohistochemistry and silver stain measures of brain β-amyloid after their death used as the reference standard. PET images were also obtained in 74 young individuals (18–50 years) presumed free of brain amyloid to better understand the frequency of a false-positive interpretation of a florbetapir-PET image. Correlation of florbetapir-PET image interpretation (based on the median of 3 nuclear medicine physicians’ ratings) and semiautomated quantification of cortical retention with postmortem β-amyloid burden, neuritic amyloid plaque density, and neuropathological diagnosis of Alzheimer disease in the first 35 participants autopsied (out of 152 individuals enrolled in the PET pathological correlation study). Florbetapir-PET imaging was performed a mean of 99 days (range, 1–377 days) before death for the 29 individuals in the primary analysis cohort. Fifteen of the 29 individuals (51.7%) met pathological criteria for Alzheimer disease. Both visual interpretation of the florbetapir-PET images and mean quantitative estimates of cortical uptake were correlated with presence and quantity of β-amyloid pathology at autopsy as measured by immunohistochemistry (Bonferroni ρ, 0.78 [95% confidence interval, 0.58–0.89]; P<.001]) and silver stain neuritic plaque score (Bonferroni ρ, 0.71 [95% confidence interval, 0.47–0.86]; P<.001). Florbetapir-PET images and postmortem results rated as positive or negative for β-amyloid agreed in 96% of the 29 individuals in the primary analysis cohort. The florbetapir-PET image was rated as amyloid negative in the 74 younger individuals in the nonautopsy cohort. Florbetapir-PET imaging was correlated with the presence and density of β-amyloid. These data provide evidence that a molecular imaging procedure can identify β-amyloid pathology in the brains of individuals during life. Additional studies are required to understand the appropriate use of florbetapir-PET imaging in the clinical diagnosis of Alzheimer disease and for the prediction of progression to dementia.
DOI: 10.1016/s0024-3205(01)01232-2
发表时间: 2001-08-17
期刊: LIFE SCIENCES
影响因子: 6.1
作者:
Klunk, WE;Wang, YM;Mathis, CA
通讯作者: Mathis, CA
DOI: 10.1016/s0197-4580(97)00057-2
发表时间: 1997-07-01
影响因子: 4.2
作者:
Ball, M;Braak, H;Khachaturian, Z
通讯作者: Khachaturian, Z
DOI: 10.1016/s1474-4422(08)70001-2
发表时间: 2008-02-01
期刊: LANCET NEUROLOGY
影响因子: 48
作者:
Rowe, Christopher C.;Ackerman, Uwe;Villemagne, Victor L.
通讯作者: Villemagne, Victor L.
DOI: 10.1056/nejm199802193380804
发表时间: 1998-02-19
影响因子: 158.5
作者:
Mayeux, R;Saunders, AM;Phelps, CH
通讯作者: Phelps, CH
DOI: 10.2967/jnumed.108.060756
发表时间: 2009-05-01
影响因子: 9.3
作者:
Koole, Michel;Lewis, Dewi M.;Van Laere, Koen
通讯作者: Van Laere, Koen