The Relation Between Brain Amyloid Deposition, Cortical Atrophy, and Plasma Biomarkers in Amnesic Mild Cognitive Impairment and Alzheimer's Disease.
The Relation Between Brain Amyloid Deposition, Cortical Atrophy, and Plasma Biomarkers in Amnesic Mild Cognitive Impairment and Alzheimer's Disease.
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DOI：
10.3389/fnagi.2018.00175
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发表时间：
2018
影响因子：
4.8
通讯作者：
Chiu MJ
中科院分区：
文献类型：
--
作者：
Fan LY;Tzen KY;Chen YF;Chen TF;Lai YM;Yen RF;Huang YY;Shiue CY;Yang SY;Chiu MJ
背景资料：神经炎性斑块和神经纤维缠结是阿尔茨海默病（AD）的病理特征，而脑淀粉样蛋白沉积在临床表现或脑萎缩中的作用尚未得到解决。我们的目的是探讨脑淀粉样蛋白沉积，皮质厚度和血浆生物标志物之间的关系。研究方法：我们使用11 C-匹兹堡化合物B-正电子发射断层扫描来测定脑淀粉样蛋白沉积，磁共振成像来估计皮质厚度，免疫磁性还原测定来测量血浆生物标志物。我们招募了39名对照组，25名遗忘型轻度认知障碍（aMCI）受试者和16名AD受试者。PiB阳性（PiB+）定义为6个预定义区域的平均皮质SUVR的95%置信区间上限（本研究中为1.0511）。结果：所有血浆生物标志物均显示出显著的组间差异。血浆Aβ40水平与PiB+和PiB-受试者的平均皮质厚度呈正相关。PiB+者血浆Aβ40水平与脑淀粉样蛋白沉积呈负相关。此外，在PiB+和PiB-受试者中，血浆tau水平与皮质厚度呈负相关。此外，皮质厚度与PiB+受试者的脑淀粉样蛋白沉积呈负相关。此外，用于区分对照和AD的血浆tau的截止点在PiB-组中高于PiB+组（分别为37.5和25.6 pg/ml）。最后，ApoE 4增加aMCI和对照组中的PiB+率。结论：脑淀粉样蛋白沉积对皮质萎缩的贡献在空间上是不同的。血浆Aβ40可能是减少脑淀粉样蛋白沉积和皮质萎缩的保护性指标。在没有脑淀粉样蛋白沉积的受试者中，需要更多的tau病理才能达到相同的认知下降水平，并且ApoE 4在淀粉样蛋白发病机制中起早期作用。
Background: Neuritic plaques and neurofibrillary tangles are the pathological hallmarks of Alzheimer’s disease (AD), while the role of brain amyloid deposition in the clinical manifestation or brain atrophy remains unresolved. We aimed to explore the relation between brain amyloid deposition, cortical thickness, and plasma biomarkers. Methods: We used 11C-Pittsburgh compound B-positron emission tomography to assay brain amyloid deposition, magnetic resonance imaging to estimate cortical thickness, and an immunomagnetic reduction assay to measure plasma biomarkers. We recruited 39 controls, 25 subjects with amnesic mild cognitive impairment (aMCI), and 16 subjects with AD. PiB positivity (PiB+) was defined by the upper limit of the 95% confidence interval of the mean cortical SUVR from six predefined regions (1.0511 in this study). Results: All plasma biomarkers showed significant between-group differences. The plasma Aβ40 level was positively correlated with the mean cortical thickness of both the PiB+ and PiB- subjects. The plasma Aβ40 level of the subjects who were PiB+ was negatively correlated with brain amyloid deposition. In addition, the plasma tau level was negatively correlated with cortical thickness in both the PiB+ and PiB- subjects. Moreover, cortical thickness was negatively correlated with brain amyloid deposition in the PiB+ subjects. In addition, the cut-off point of plasma tau for differentiating between controls and AD was higher in the PiB- group than in the PiB+ group (37.5 versus 25.6 pg/ml, respectively). Lastly, ApoE4 increased the PiB+ rate in the aMCI and control groups. Conclusion: The contributions of brain amyloid deposition to cortical atrophy are spatially distinct. Plasma Aβ40 might be a protective indicator of less brain amyloid deposition and cortical atrophy. It takes more tau pathology to reach the same level of cognitive decline in subjects without brain amyloid deposition, and ApoE4 plays an early role in amyloid pathogenesis.
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影响因子：
3.7
作者：
Blennow K
通讯作者：
Blennow K
影响因子：
3.7
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Dickerson, Bradford C.;Bakkour, Akram;Salat, David H.;Feczko, Eric;Pacheco, Jenni;Greve, Douglas N.;Grodstein, Fran;Wright, Christopher I.;Blacker, Deborah;Rosas, H. Diana;Sperling, Reisa A.;Atri, Alireza;Growdon, John H.;Hyman, Bradley T.;Morris, John C.;Fischl, Bruce;Buckner, Randy L.
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Buckner, Randy L.
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通讯作者：
Raussens, Vincent
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4.8
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Lee NC;Yang SY;Chieh JJ;Huang PT;Chang LM;Chiu YN;Huang AC;Chien YH;Hwu WL;Chiu MJ
通讯作者：
Chiu MJ
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4.8
作者：
Cudaback, Eiron;Li, Xianwu;Keene, C. Dirk
通讯作者：
Keene, C. Dirk