Lack of association between 11C-PiB and longitudinal brain atrophy in non-demented older individuals.

Lack of association between 11C-PiB and longitudinal brain atrophy in non-demented older individuals.
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DOI:
10.1016/j.neurobiolaging.2009.12.008
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发表时间:
2011-12
影响因子:
4.2
通讯作者:
Resnick, Susan M.
Resnick, Susan M.
中科院分区:
医学2区
文献类型:
--
作者:
Driscoll, Ira;Zhou, Yun;An, Yang;Sojkova, Jitka;Davatzikos, Christos;Kraut, Michael A.;Ye, Weiguo;Ferrucci, Luigi;Mathis, Chester A.;Klunk, William E.;Wong, Dean F.;Resnick, Susan M.

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β 淀粉样蛋白斑块 (Aβ) 是阿尔茨海默病 (AD) 的一个标志,在疾病初期几十年前就开始沉积,并被认为与神经元损失、脑萎缩和认知障碍有关。我们在 57 名非痴呆个体(年龄 64-86;M = 78.7)中检查了 11C-PiB-PET 测量的 Aβ 负荷与前几年脑体积变化之间的关联。参与者通过巴尔的摩纵向衰老研究进行前瞻性随访,最多进行 10 次连续 MRI 扫描 (M = 8.1),并在初次 MRI 大约 10 年后进行 11C-PiB 扫描。使用线性混合效应模型来确定平均皮质 11C-PiB 分布体积比(通过将参考组织模型拟合到测量的时间活动曲线来估计)是否与全脑、脑室脑脊液、额叶、颞叶、顶叶和枕叶白质和灰质、海马体、眶额皮质和楔前叶的纵向区域脑体积变化相关。尽管所有研究区域的体积均显着纵向下降(p < 0.05),但当前 Aβ 负荷与前几年区域脑体积下降轨迹之间没有检测到关联,Aβ 负荷最高和最低的区域之间的区域体积轨迹也没有差异。与疾病阈值模型一致,我们的研究结果表明,Aβ 负荷似乎不会影响未患痴呆症的个体的脑容量变化。
Amyloid-β plaques (Aβ) are a hallmark of Alzheimer's disease (AD), begin deposition decades before the incipient disease, and are thought to be associated with neuronal loss, brain atrophy and cognitive impairment. We examine associations between 11C-PiB-PET measurement of Aβ burden and brain volume changes in the preceding years in 57 non-demented individuals (age 64-86; M = 78.7). Participants were prospectively followed through the Baltimore Longitudinal Study of Aging, with up to 10 consecutive MRI scans (M = 8.1) and an 11C-PiB scan approximately 10 years after the initial MRI. Linear mixed effects models were used to determine whether mean cortical 11C-PiB distribution volume ratios, estimated by fitting a reference tissue model to the measured time activity curves, were associated with longitudinal regional brain volume changes of the whole brain, ventricular CSF, frontal, temporal, parietal, and occipital white and gray matter, the hippocampus, orbito-frontal cortex, and the precuneus. Despite significant longitudinal declines in the volumes of all investigated regions (p < 0.05), no associations were detected between current Aβ burden and regional brain volume decline trajectories in the preceding years, nor did the regional volume trajectories differ between those with highest and lowest Aβ burden. Consistent with a threshold model of disease, our findings suggest that Aβ load does not seem to affect brain volume changes in individuals without dementia.
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