Purpose

Default mode network (DMN) has emerged as a potential biomarker of Alzheimer’s disease (AD); however, it is not clear whether it can differentiate amnestic mild cognitive impairment with altered amyloid (aMCI-Aβ +) who will evolve to AD. We evaluated if structural and functional connectivity (FC), hippocampal volumes (HV), and cerebrospinal fluid biomarkers (CSF—Aβ₄₂, p-Tau, and t-Tau) can differentiate aMCI-Aβ + converters from non-converters.

Methods

Forty-eight individuals (18 normal controls and 30 aMCI subjects in the AD continuum — with altered Aβ₄₂ in the CSF) were followed up for an average of 13 months. We used MultiAtlas, UF²C, and Freesurfer software to evaluate diffusion tensor imaging, FC, and HV, respectively, INNOTEST® kits to measure CSF proteins, and neuropsychological tests. Besides, we performed different MANOVAs with further univariate analyses to differentiate groups.

Results

During follow-up, 8/30 aMCI-Aβ + converted (26.6%) to AD dementia. There were no differences in multivariate analysis between groups in CSF biomarkers (p = 0.092) or at DMN functional connectivity (p = 0.814). aMCI-Aβ + converters had smaller right HV than controls (p = 0.013), and greater right cingulum parahippocampal bundle radial diffusivity than controls (p < 0.001) and non-converters (p = 0.036).

Conclusion

In this exploratory study, structural, but not functional, DMN connectivity alterations may differentiate aMCI-Aβ + subjects who converted to AD dementia.

中文翻译：

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淀粉样蛋白阳性轻度认知障碍中结构和功能默认模式网络连接的差异：一项纵向研究

目的

默认模式网络 (DMN) 已成为阿尔茨海默病 (AD) 的潜在生物标志物；然而，尚不清楚它是否可以区分具有改变的淀粉样蛋白（aMCI-Aβ+）的遗忘型轻度认知障碍，后者将演变为 AD。我们评估了结构和功能连接 (FC)、海马体积 (HV) 和脑脊液生物标志物（CSF-Aβ ₄₂、p-Tau 和 t-Tau）是否可以区分 aMCI-Aβ + 转换器和非转换器。

方法

48 名个体（18 名正常对照和 30 名 aMCI 受试者在 AD 连续体中——脑脊液中的Aβ ₄₂改变）平均随访 13 个月。我们分别使用 MultiAtlas、UF ² C 和 Freesurfer 软件评估扩散张量成像、FC 和 HV，使用 INNOTEST® 套件测量 CSF 蛋白和神经心理学测试。此外，我们通过进一步的单变量分析进行了不同的多元方差分析以区分组。

结果

在随访期间，8/30 aMCI-Aβ + 转换 (26.6%) 为 AD 痴呆。在 CSF 生物标志物 (p = 0.092) 或 DMN 功能连接 ( p  = 0.814)方面，组间多变量分析没有差异。aMCI-Aβ + 转换器的右侧 HV 比对照组小 ( p  = 0.013)，右侧扣带回海马旁束径向扩散率大于对照组 ( p  < 0.001) 和非转换器 ( p  = 0.036)。

结论

在这项探索性研究中，结构性而非功能性 DMN 连接性改变可能会区分转化为 AD 痴呆的 aMCI-Aβ + 受试者。