Abdullah Laila, Paris Daniel, Luis Cheryl, Quadros Amita, Parrish Julia, Valdes Luis, Keegan Andrew P, Mathura Venkatarajan, Crawford Fiona, Mullan Michael
Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, United States.
Neurosci Lett. 2007 Nov 27;428(2-3):53-8. doi: 10.1016/j.neulet.2007.09.058. Epub 2007 Oct 2.
Evidence suggests that high peripheral beta-amyloid (Abeta)(1-40) levels and low ratios of Abeta(1-42)/Abeta(1-40) are associated with increased risk for Alzheimer's disease (AD). In this cross-sectional design, serum and plasma samples from 67 AD patients and 146 controls (similar in age and gender) were evaluated using Abeta(1-40) and Abeta(1-42) ELISA. Coefficient of variance was calculated for intra- and inter-person variability of Abeta(1-40) and Abeta(1-42). Abeta(1-40) correlated with age, MMSE and their Abeta(1-42)/Abeta(1-40) ratios (p<0.05). Significantly higher Abeta(1-40) levels were observed in AD patients than controls (p<0.05) but no difference was observed for Abeta(1-42) (p>0.05). Serum Abeta(1-42)/Abeta(1-40) ratios were also significantly lower in AD patients than controls (p<0.05). Lower intra-person than inter-person variability was observed for serum and plasma Abeta(1-40) and Abeta(1-42) and these were higher in controls than in AD patients. The intra-person variability of serum Abeta(1-40) did not influence the group differences observed between AD patients and controls. Significant interaction was observed between diagnosis and intra-person variability for serum Abeta(1-40) levels (p<0.05) and was supported by our finding of higher intra-person variability for serum Abeta(1-40) in controls (26.97%) than in AD patients (18.35%). We confirm the previously observed differences in blood Abeta levels between AD and control groups. In addition, we now report the presence of high intra- and inter-person variability possibly due to factors that influence peripheral Abeta levels and warrant further investigation before the potential use of Abeta as an AD biomarker can be fully exploited.
有证据表明，外周β-淀粉样蛋白（Aβ）（1-40）水平升高以及Aβ（1-42）/Aβ（1-40）比例降低与阿尔茨海默病（AD）风险增加相关。在这项横断面设计中，使用Aβ（1-40）和Aβ（1-42）酶联免疫吸附测定法（ELISA）对67例AD患者和146例（年龄和性别匹配）对照者的血清和血浆样本进行了评估。计算了Aβ（1-40）和Aβ（1-42）的人际内和人际间变异系数。Aβ（1-40）与年龄、简易精神状态检查表（MMSE）及其Aβ（1-42）/Aβ（1-40）比例相关（p<0.05）。AD患者的Aβ（1-40）水平显著高于对照者（p<0.05），但Aβ（1-42）水平无差异（p>0.05）。AD患者的血清Aβ（1-42）/Aβ（1-40）比例也显著低于对照者（p<0.05）。血清和血浆Aβ（1-40）及Aβ（1-42）的人际内变异低于人际间变异，且对照者的变异高于AD患者。血清Aβ（1-40）的人际内变异不影响AD患者与对照者之间观察到的组间差异。血清Aβ（1-40）水平在诊断与人际内变异之间观察到显著交互作用（p<0.05），且我们发现对照者血清Aβ（1-40）的人际内变异（26.97%）高于AD患者（18.35%），支持了这一结果。我们证实了之前观察到的AD组与对照组血液Aβ水平的差异。此外，我们现在报告存在较高的人际内和人际间变异，这可能是由于影响外周Aβ水平的因素所致，在Aβ作为AD生物标志物的潜在用途得到充分利用之前，值得进一步研究。
