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首页> 外文期刊>NeuroImage: Clinical >Does amyloid deposition produce a specific atrophic signature in cognitively normal subjects?
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Does amyloid deposition produce a specific atrophic signature in cognitively normal subjects?

机译：淀粉样蛋白沉积在认知正常受试者中会产生特定的萎缩签名吗？

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The objective of our study was to evaluate whether cognitively normal (CN) elderly participants showing elevated cortical beta-amyloid (Aβ) deposition have a consistent neuroanatomical signature of brain atrophy that may characterize preclinical Alzheimer's disease (AD). 115 CN participants who were Aβ-positive (CN+) by amyloid PET imaging; 115 CN participants who were Aβ-negative (CN?); and 88 Aβ-positive mild cognitive impairment or AD participants (MCI/AD+) were identified. Cortical thickness (FreeSurfer) and gray matter volume (SPM5) were measured for 28 regions-of-interest (ROIs) across the brain and compared across groups. ROIs that best discriminated CN? from CN+ differed for FreeSurfer cortical thickness and SPM5 gray matter volume. Group-wise discrimination was poor with a high degree of uncertainty in terms of the rank ordering of ROIs. In contrast, both techniques showed strong and consistent findings comparing MCI/AD+ to both CN? and CN+ groups, with entorhinal cortex, middle and inferior temporal lobe, inferior parietal lobe, and hippocampus providing the best discrimination for both techniques. Concordance across techniques was higher for the CN? and CN+ versus MCI/AD+ comparisons, compared to the CN? versus CN+ comparison. The weak and inconsistent nature of the findings across technique in this study cast doubt on the existence of a reliable neuroanatomical signature of preclinical AD in elderly PiB-positive CN participants. Highlights ? We measured atrophy in cognitively normal subjects with amyloid deposition (CN+). ? Findings in CN+ subjects were weak and disconcordant across Freesurfer and SPM5. ? Concordance across techniques was higher when assessing Alzheimer disease subjects. ? Evidence for a neuroanatomical signature of preclinical AD in CN+ subjects is weak.
机译：我们研究的目的是评估显示皮层β-淀粉样蛋白（Aβ）沉积升高的认知正常（CN）老年参与者是否具有一致的脑萎缩神经解剖学特征，该特征可能是临床前阿尔茨海默氏病（AD）的特征。 115名通过淀粉样蛋白PET成像呈Aβ阳性（CN +）的CN参与者; 115名Aβ阴性（CN？）的CN参与者;确定了88位Aβ阳性轻度认知障碍或AD参与者（MCI / AD +）。测量了大脑中28个感兴趣区域（ROI）的皮质厚度（FreeSurfer）和灰质体积（SPM5），并在各组之间进行了比较。最能区分CN的ROI？ CN +的FreeSurfer皮质厚度和SPM5灰质体积有所不同。就ROI的等级排序而言，基于组的区分很差，不确定性很高。相反，将MCI / AD +与两种CN？相比，两种技术均显示出了强大而一致的发现。和CN +组，其内嗅皮层，颞中叶和下颞叶，顶叶下叶和海马为这两种技术提供了最佳区分。 CN的跨技术一致性更高？以及CN +与MCI / AD +的比较，以及CN？与CN +比较。在这项研究中，跨技术发现的弱和不一致的性质使人们怀疑PiB阳性CN老年参与者临床前AD是否存在可靠的神经解剖学特征。强调 ？我们在淀粉样蛋白沉积（CN +）的认知正常受试者中测量了萎缩。 ？在Freesurfer和SPM5中，CN +主题的发现薄弱且不一致。 ？评估阿尔茨海默病受试者时，各种技术的一致性更高。 ？在CN +受试者中临床前AD的神经解剖学特征的证据很少。

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