NIH Biomedical Research Center, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA.
Neurobiol Aging. 2011 Dec;32(12):2123-30. doi: 10.1016/j.neurobiolaging.2009.12.008. Epub 2010 Feb 21.
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 (11)C-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 (11)C-PiB scan approximately 10 years after the initial MRI. Linear mixed effects models were used to determine whether mean cortical (11)C-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.
淀粉样蛋白-β斑块（Aβ）是阿尔茨海默病（AD）的标志，在疾病初期出现之前几十年就开始沉积，并被认为与神经元丧失、脑萎缩和认知障碍有关。我们检查了 57 名非痴呆个体（年龄 64-86 岁；M=78.7）中 Aβ 负担的（11）C-PiB-PET 测量值与前几年大脑体积变化之间的关联。参与者通过巴尔的摩纵向研究进行前瞻性随访，最多进行了 10 次连续的 MRI 扫描（M=8.1），并且在初始 MRI 后大约 10 年进行了（11）C-PiB 扫描。线性混合效应模型用于确定通过拟合参考组织模型来测量时间活动曲线估计的平均皮质（11）C-PiB 分布体积比是否与整个大脑、脑室 CSF、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都有显著的纵向下降（p<0.05），但当前 Aβ 负担与前几年的区域脑体积下降轨迹之间没有发现关联，也没有发现 Aβ 负担最高和最低的个体之间的区域体积轨迹存在差异。与疾病的阈值模型一致，我们的研究结果表明，在没有痴呆的个体中，Aβ 负荷似乎不会影响大脑体积的变化。
