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阿尔茨海默病中淀粉样蛋白毒性的体内图谱

In vivo mapping of amyloid toxicity in Alzheimer disease.

作者信息

Frisoni G B, Lorenzi M, Caroli A, Kemppainen N, Någren K, Rinne J O

机构信息

Laboratory of Epidemiology and Neuroimaging, IRCCS San Giovanni di Dio-FBF, via Pilastroni 4, I-25123 Brescia, Italy.

出版信息

Neurology. 2009 Apr 28;72(17):1504-11. doi: 10.1212/WNL.0b013e3181a2e896.

DOI:10.1212/WNL.0b013e3181a2e896
PMID:19398705
Abstract

OBJECTIVE

To study the relationship between gray matter atrophy and amyloid deposition in Alzheimer disease (AD).

METHODS

Volumetric magnetic resonance (MR) and [11C]-PIB PET were acquired from 23 patients with AD and 17 healthy older persons. Standardized [11C]-PIB uptake values were coregistered to MR scans in a standard space. Decreased density of and increased [11C]-PIB uptake in the gray matter of patients with AD vs controls were assessed with both voxel-based (p < 0.05 corrected) and region-of-interest (ROI) analyses. The relationship between decreased density of and increased [11C]-PIB uptake in the gray matter was investigated with voxel-based Pearson r maps (thresholded at p < 0.05) and ROI linear regression plots.

RESULTS

Atrophy mapped to the hippocampus and increased [11C]-PIB uptake to large frontal, parietal, and posterior cingulate cortical areas. ROI analysis showed the largest effect size for atrophy in the hippocampus (2.01) and amygdala (1.27) and the highest effect size for [11C]-PIB uptake in frontal (2.66), posterior cingulate/retrosplenial (2.43), insular (2.41), and temporal (2.23) regions. In the hippocampus, [11C]-PIB uptake was significantly increased, but effect size was milder (1.72). Significant correlations between atrophy and increased [11C]-PIB uptake were found in the hippocampal (r = -0.54) and amygdalar ROIs (r = -0.40) but not in the frontal, temporal, posterior cingulate/retrosplenial, insular, and caudate ROIs (r between 0.04 and 0.25).

CONCLUSION

The medial temporal lobe might be highly susceptible to amyloid toxicity, whereas neocortical areas might be more resilient.

摘要

目的

研究阿尔茨海默病(AD)中灰质萎缩与淀粉样蛋白沉积之间的关系。

方法

对23例AD患者和17名健康老年人进行容积磁共振(MR)和[11C] - PIB PET检查。标准化的[11C] - PIB摄取值在标准空间中与MR扫描进行配准。采用基于体素(校正p < 0.05)和感兴趣区(ROI)分析评估AD患者与对照组相比灰质密度降低和[11C] - PIB摄取增加的情况。通过基于体素的Pearson r图(阈值设定为p < 0.05)和ROI线性回归图研究灰质密度降低与[11C] - PIB摄取增加之间的关系。

结果

萎缩定位于海马体,[11C] - PIB摄取增加定位于额叶、顶叶和后扣带回皮质大区域。ROI分析显示海马体(2.01)和杏仁核(1.27)萎缩的效应量最大,额叶(2.66)、后扣带回/楔前叶(2.43)、岛叶(2.41)和颞叶(2.23)区域[11C] - PIB摄取的效应量最高。在海马体中,[11C] - PIB摄取显著增加,但效应量较小(1.72)。在海马体ROI(r = -0.54)和杏仁核ROI(r = -0.40)中发现萎缩与[11C] - PIB摄取增加之间存在显著相关性,但在额叶、颞叶、后扣带回/楔前叶、岛叶和尾状核ROI中未发现(r在0.04至0.25之间)。

结论

内侧颞叶可能对淀粉样蛋白毒性高度敏感,而新皮质区域可能更具弹性。

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