Blood Beta-Amyloid and Tau in Down Syndrome: A Comparison with Alzheimer's Disease.
Blood Beta-Amyloid and Tau in Down Syndrome: A Comparison with Alzheimer's Disease.
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DOI：
10.3389/fnagi.2016.00316
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发表时间：
2016
影响因子：
4.8
通讯作者：
Chiu MJ
中科院分区：
文献类型：
--
作者：
Lee NC;Yang SY;Chieh JJ;Huang PT;Chang LM;Chiu YN;Huang AC;Chien YH;Hwu WL;Chiu MJ
背景资料：在阿尔茨海默病（AD）患者以及唐氏综合征（DS）和AD患者中已经注意到β-淀粉样蛋白（Aβ）和tau蛋白的变化。然而，报告的变化，在早期阶段的回归，如行为和精神症状的痴呆症（BPSD），在DS是稀疏的。研究方法：对照组78例，AD组62例，DS组35例，DS伴变性（DS_D）组16例，其中BPSD组9例，痴呆组7例。采用免疫磁性还原法（IMR）分析血液中β-淀粉样蛋白40和42（Aβ-40，Aβ-42）和tau蛋白的水平。采用适应性行为痴呆问卷（ABDQ）评估患者的临床状况。结果：与对照组相比，DS组Aβ-40和tau水平升高，A β-42水平和Aβ-42/Aβ-40比值降低（均P < 0.001）。与无变性的DS相比，DS_D中观察到A β-40水平降低和A β-42水平升高以及Aβ-42/40比值升高（均p < 0.001）。ABDQ评分与Aβ-40水平（ρ =-0.556）和tau蛋白水平（ρ =-0.410）呈负相关，与Aβ-42水平（ρ = 0.621）和Aβ-42/40比值（ρ = 0.544;均p < 0.05）呈正相关。结论：Aβ-40、Aβ-42水平及A β-42/Aβ-40比值可作为早期检测DS退行性变的生物标志物。DS中Aβ-40和tau水平升高可能提示早期神经退行性变。DS_D中Aβ-42的增加可能反映了Aβ-42的神经毒性。在DS_D中tau蛋白减少的悖论可以用长期神经退行性变过程中的倦怠现象来解释。血浆β-淀粉样蛋白和tau蛋白的不同模式可能意味着在一般人群中，尽管具有共同的关键病理学特征，但退行性DS和AD之间存在不同的发病机制。
Background: Changes in β-amyloids (Aβ) and tau proteins have been noted in patients with Alzheimer’s disease (AD) and patients with both Down syndrome (DS) and AD. However, reports of changes in the early stage of regression, such as behavioral and psychological symptoms of dementia (BPSD), in DS are sparse. Methods: Seventy-eight controls, 62 patients with AD, 35 with DS and 16 with DS with degeneration (DS_D), including 9 with BPSD and 7 with dementia, were enrolled. The levels of β-amyloids 40 and 42 (Aβ-40, Aβ-42) and tau protein in the blood were analyzed using immunomagnetic reduction (IMR). The Adaptive Behavior Dementia Questionnaire (ABDQ) was used to evaluate the clinical status of the degeneration. Results: The Aβ-40 and tau levels were higher and the Aβ-42 level and Aβ-42/Aβ-40 ratio were lower in DS than in the controls (all p < 0.001). Decreased Aβ-40 and increased Aβ-42 levels and Aβ-42/40 ratios were observed in DS_D compared with DS without degeneration (all p < 0.001). The ABDQ score was negatively correlated with the Aβ-40 level (ρ = −0.556) and the tau protein level (ρ = −0.410) and positively associated with the Aβ-42 level (ρ = 0.621) and the Aβ-42/40 ratio (ρ = 0.544; all p < 0.05). Conclusions: The Aβ-40 and Aβ-42 levels and the Aβ-42/Aβ-40 ratio are considered possible biomarkers for the early detection of degeneration in DS. The elevated Aβ-40 and tau levels in DS may indicate early neurodegeneration. The increased Aβ-42 in DS_D may reflect the neurotoxicity of Aβ-42. The paradox of the tau decreases in DS_D could be explained by a burnout phenomenon during long-term neurodegeneration. The different patterns of the plasma beta amyloids and tau protein may imply a different pathogenesis between DS with degeneration and AD in the general population, in spite of their common key pathological features.