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早老素 1 突变携带者中淀粉样蛋白沉积的碳-11-匹兹堡化合物 B 正电子发射断层扫描成像。

Carbon-11-Pittsburgh compound B positron emission tomography imaging of amyloid deposition in presenilin 1 mutation carriers.

机构信息

Department of Neurodegeneration, UCL Institute of Neurology, University College London, Dementia Research Centre, Queen Square, London WC1N 3BG, UK.

出版信息

Brain. 2011 Jan;134(Pt 1):293-300. doi: 10.1093/brain/awq310. Epub 2010 Nov 16.

Abstract

(11)Carbon-Pittsburgh compound B positron emission tomography studies have suggested early and prominent amyloid deposition in the striatum in presenilin 1 mutation carriers. This cross-sectional study examines the (11)Carbon-Pittsburgh compound B positron emission tomography imaging profiles of presymptomatic and mildly affected (mini-mental state examination ≥ 20) carriers of seven presenilin 1 mutations, comparing them with groups of controls and symptomatic sporadic Alzheimer's disease cases. Parametric ratio images representing (11)Carbon-Pittsburgh compound B retention from 60 to 90 min were created using the pons as a reference region and nine regions of interest were studied. We confirmed that increased amyloid load may be detected in presymptomatic presenilin 1 mutation carriers with (11)Carbon-Pittsburgh compound B positron emission tomography and that the pattern of retention is heterogeneous. Comparison of presenilin 1 and sporadic Alzheimer's disease groups revealed significantly greater thalamic retention in the presenilin 1 group and significantly greater frontotemporal retention in the sporadic Alzheimer's disease group. A few individuals with presenilin 1 mutations showed increased cerebellar (11)Carbon-Pittsburgh compound B retention suggesting that this region may not be as suitable a reference region in familial Alzheimer's disease.

摘要

(11)Carbon-Pittsburgh 化合物 B 正电子发射断层扫描研究表明,早老素 1 突变携带者纹状体中淀粉样蛋白沉积明显。这项横断面研究比较了七名早老素 1 突变携带者的无症状和轻度受影响(迷你精神状态检查≥20)者以及对照组和症状性散发性阿尔茨海默病病例的(11)Carbon-Pittsburgh 化合物 B 正电子发射断层扫描成像特征。使用桥脑作为参照区创建了代表(11)Carbon-Pittsburgh 化合物 B 保留的 60 至 90 分钟的参数比值图像,并研究了九个感兴趣区。我们证实,(11)Carbon-Pittsburgh 化合物 B 正电子发射断层扫描可检测无症状早老素 1 突变携带者中淀粉样蛋白负荷增加,且保留模式呈异质性。早老素 1 组和散发性阿尔茨海默病组的比较显示,早老素 1 组丘脑保留明显增加,散发性阿尔茨海默病组额颞叶保留明显增加。一些早老素 1 突变携带者的小脑(11)Carbon-Pittsburgh 化合物 B 保留增加,提示该区域在家族性阿尔茨海默病中可能不是一个合适的参照区。

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