[11]PIB in a nondemented population -: Potential antecedent marker of Alzheimer disease
[11]PIB in a nondemented population -: Potential antecedent marker of Alzheimer disease
复制标题
DOI：
10.1212/01.wnl.0000228230.26044.a4
复制
发表时间：
2006-08-08
期刊：
影响因子：
9.9
通讯作者：
Morris, J. C.
中科院分区：
文献类型：
--
作者：
Mintun, M. A.;LaRossa, G. N.;Morris, J. C.
背景：β-淀粉样蛋白（A β）斑块是阿尔茨海默病（AD）的标志.与体内A β斑块结合的PET成像示踪剂，N-甲基-[C-11]2-（4=-甲基氨基苯基）-6-羟基苯并噻唑（或[C-11]PIB，“匹兹堡化合物-B”），与非痴呆对照相比，在被诊断患有阿尔茨海默型痴呆（DAT）的受试者中具有显著更高的结合。作者使用这种成像技术来研究在认知变化发展之前，临床正常个体是否发生异常结合。研究方法：41例非痴呆受试者（年龄范围20 - 86岁）和10例DAT患者（年龄范围66 - 86岁）接受了[C-11] PIB PET扫描。在MRI上绘制了小脑、前额叶、颞叶外侧、枕叶、直回、楔前叶和纹状体皮质上的感兴趣区域。使用Logan图形分析和参考组织的小脑皮质计算与[C-11]PIB-A β结合位点密度成比例的结合电位值（BP）。结果：DAT患者的血压值高于非痴呆受试者（p < 0.0001）。41名非痴呆受试者中有4名皮质BP值升高，他们的BP值作为一个组与DAT受试者的BP值没有显著差异。这4例非痴呆受试者中有2例的[C-11] PIB摄取（目视和定量）与DAT受试者无法区分。结论：在非痴呆受试者中升高的[C-11] PIB结合表明[C-11] PIB淀粉样蛋白成像可能对临床前阿尔茨海默病状态的检测敏感。需要进行纵向研究，以确定[C-11] PIB结合升高与阿尔茨海默型痴呆发生风险之间的关系。
Background: Beta- amyloid (A beta) plaques are the hallmark of Alzheimer disease (AD). A PET imaging tracer that binds to A beta plaques in vivo, N-methyl-[C-11]2-(4=-methylaminophenyl)-6-hydroxybenzothiazole ( or [C-11]PIB for "Pittsburgh Compound-B"), has significantly higher binding in subjects diagnosed with dementia of the Alzheimer type (DAT) compared to nondemented controls. The authors used this imaging technique to investigate whether abnormal binding occurs in clinically normal individuals, prior to the development of cognitive changes. Methods: Forty-one nondemented subjects ( age range 20 to 86 years) and 10 patients with DAT ( age range 66 to 86 years) underwent [C-11] PIB PET scanning. Regions of interest were drawn on the MRI over the cerebellar, prefrontal, lateral temporal, occipital, gyrus rectus, precuneus, and striatal cortex. Binding potential values (BPs), proportional to the density of [C-11]PIB-A beta binding sites, were calculated using the Logan graphical analysis and the cerebellar cortex for a reference tissue. Results: Patients with DAT had elevated BP values vs nondemented subjects (p < 0.0001). Four of the 41 nondemented subjects had elevated cortical BP values and their BP values as a group were not significantly different from the DAT subjects' BP values. Two of these four nondemented subjects had [C-11] PIB uptake, both visually and quantitatively, that was indistinguishable from the DAT subjects. Conclusions: Elevated [C-11] PIB binding in nondemented subjects suggests that [C-11] PIB amyloid imaging may be sensitive for detection of a preclinical Alzheimer disease state. Longitudinal studies will be required to determine the association of elevated [C-11] PIB binding and risk of developing dementia of the Alzheimer type.