Principal component analysis of PiB distribution in Parkinson and Alzheimer diseases

Principal component analysis of PiB distribution in Parkinson and Alzheimer diseases
复制标题

DOI:
10.1212/wnl.0b013e31829e6f94
复制
发表时间:
2013-08-06
期刊:
影响因子:
9.9
通讯作者:
Perlmutter, Joel S.
Perlmutter, Joel S.
中科院分区:
医学1区
文献类型:
--
作者:
Campbell, Meghan C.;Markham, Joanne;Perlmutter, Joel S.

文献摘要

被引文献

相似文献

目的:采用匹兹堡化合物B(PiB)PET成像的主成分分析(PCA),以确定帕金森病(PD)伴认知障碍患者体内β-淀粉样蛋白(A β)的模式是否与症状性阿尔茨海默病(AD)中发现的模式相似。PiB PET扫描来自PD伴认知障碍的参与者(n = 53),症状性AD的参与者(n = 5 - 35)和年龄匹配的对照组(n = 67)。所有人都使用临床痴呆评级进行评估,并在137名参与者中确定了APOE基因型。PCA用于1)确定AD中的PiB结合模式,2)确定可能的独特PD模式,和3)直接比较PD和AD组中的PiB结合模式。PD伴认知障碍的参与者与症状性AD参与者在两个方面也有显著差异(p < 0.001)。然而,PD组和对照组的任一组分均无差异。即使是那些参与者与PD与升高的平均皮层结合电位显着不同的参与者与AD上的两个component.Conclusion:使用PCA,我们表明,参与者与PD与认知障碍不表现出相同的PiB结合模式与AD的参与者。这些数据表明,抗体沉积可能发挥不同的病理生理作用的认知功能障碍的PD相比,在AD。
Objective: To use principal component analyses (PCA) of Pittsburgh compound B (PiB) PET imaging to determine whether the pattern of in vivo beta-amyloid (A beta) in Parkinson disease (PD) with cognitive impairment is similar to the pattern found in symptomatic Alzheimer disease (AD).Methods: PiB PET scans were obtained from participants with PD with cognitive impairment (n = 53), participants with symptomatic AD (n 5 35), and age-matched controls (n = 67). All were assessed using the Clinical Dementia Rating and APOE genotype was determined in 137 participants. PCA was used to 1) determine the PiB binding pattern in AD, 2) determine a possible unique PD pattern, and 3) directly compare the PiB binding patterns in PD and AD groups.Results: The first 2 principal components (PC1 and PC2) significantly separated the AD and control participants (p < 0.001). Participants with PD with cognitive impairment also were significantly different from participants with symptomatic AD on both components (p < 0.001). However, there was no difference between PD and controls on either component. Even those participants with PD with elevated mean cortical binding potentials were significantly different from participants with AD on both components.Conclusion: Using PCA, we demonstrated that participants with PD with cognitive impairment do not exhibit the same PiB binding pattern as participants with AD. These data suggest that Ab deposition may play a different pathophysiologic role in the cognitive impairment of PD compared to that in AD.