Department of Neurology, University of Pennsylvania, Philadelphia, PA, USA; Penn Image Computing and Science Laboratory, University of Pennsylvania, Philadelphia, PA, USA; Penn Memory Center, University of Pennsylvania, Philadelphia, PA, USA; Penn Alzheimer's Disease Core Center, University of Pennsylvania, Philadelphia, PA, USA.
Penn Image Computing and Science Laboratory, University of Pennsylvania, Philadelphia, PA, USA; Department of Radiology, University of Pennsylvania, Philadelphia, PA, USA.
Neurobiol Aging. 2018 Jun;66:49-58. doi: 10.1016/j.neurobiolaging.2018.01.024. Epub 2018 Feb 9.
We examined the relationship between in vivo estimates of tau deposition as measured by F-AV-1451 tau positron emission tomography imaging and cross-sectional cortical thickness, as well as rates of antecedent cortical thinning measured from magnetic resonance imaging in individuals with and without evidence of cerebral amyloid in 63 participants from the Alzheimer's Disease Neuroimaging Initiative study, including 32 cognitively normal individuals (mean age 74 years), 27 patients with mild cognitive impairment (mean age 76.8 years), and 4 patients diagnosed with Alzheimer's disease (mean age 80 years). We hypothesized that structural measures would correlate with F-AV-1451 in a spatially local manner and that this correlation would be stronger for longitudinal compared to cross-sectional measures of cortical thickness and in those with cerebral amyloid versus those without. Cross-sectional and longitudinal estimates of voxelwise atrophy were made from whole brain maps of cortical thickness and rates of thickness change. In amyloid-β-positive individuals, the correlation of voxelwise atrophy across the whole brain with a summary measure of medial temporal lobe (MTL) F-AV-1451 uptake demonstrated strong local correlations in the MTL with longitudinal atrophy that was weaker in cross-sectional analysis. Similar effects were seen in correlations between 31 bilateral cortical regions of interest. In addition, several nonlocal correlations between atrophy and F-AV-1451 uptake were observed, including association between MTL atrophy and F-AV-1451 uptake in parietal lobe regions of interest such as the precuneus. Amyloid-β-negative individuals only showed weaker correlations in data uncorrected for multiple comparisons. While these data replicate previous reports of associations between F-AV-1451 uptake and cross-sectional structural measures, the current results demonstrate a strong relationship with longitudinal measures of atrophy. These data support the notion that in vivo measures of tau pathology are tightly linked to the rate of neurodegenerative change.
我们研究了 63 名来自阿尔茨海默病神经影像学倡议研究的个体中，体内 tau 沉积的活体估计值与皮质厚度的横断面之间的关系，以及磁共振成像测量的皮质变薄的先行率，这些个体中有或没有脑淀粉样蛋白的证据，包括 32 名认知正常个体（平均年龄 74 岁）、27 名轻度认知障碍患者（平均年龄 76.8 岁）和 4 名阿尔茨海默病患者（平均年龄 80 岁）。我们假设结构测量值将以空间局部的方式与 F-AV-1451 相关，并且这种相关性在皮质厚度的纵向测量值与横断面测量值相比以及在有脑淀粉样蛋白的个体与无脑淀粉样蛋白的个体相比会更强。从皮质厚度和厚度变化率的全脑图谱中得出了体素萎缩的横断面和纵向估计值。在淀粉样蛋白-β阳性个体中，全脑体素萎缩与内侧颞叶（MTL）F-AV-1451 摄取的综合测量值之间的相关性显示，MTL 中的纵向萎缩具有很强的局部相关性，而在横断面分析中则较弱。在 31 个双侧皮质感兴趣区之间的相关性中也观察到了类似的效果。此外，还观察到了萎缩和 F-AV-1451 摄取之间的几个非局部相关性，包括 MTL 萎缩与顶叶感兴趣区（如楔前叶）的 F-AV-1451 摄取之间的关联。未经多次比较校正的数据仅显示出淀粉样蛋白-β阴性个体的相关性较弱。虽然这些数据复制了之前报道的 F-AV-1451 摄取与横断面结构测量值之间的关联，但目前的结果表明与萎缩的纵向测量值之间存在很强的关系。这些数据支持这样一种观点，即体内 tau 病理学的测量值与神经退行性变化的速度密切相关。
