Meta-analysis of plasma amyloid-β levels in Alzheimer's disease.

Meta-analysis of plasma amyloid-β levels in Alzheimer's disease.
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DOI:
10.3233/jad-2011-101977
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发表时间:
2011
期刊:
Journal of Alzheimer's disease : JAD
影响因子:
--
通讯作者:
Sachdev PS
Sachdev PS
中科院分区:
其他
文献类型:
--
作者:
Song F;Poljak A;Valenzuela M;Mayeux R;Smythe GA;Sachdev PS

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血浆淀粉样蛋白-β (Aβ) 水平已被提议作为阿尔​​茨海默病 (AD) 的生物标志物,但研究得出的结果不一致。我们对横断面研究(检查 AD 和认知正常受试者的血浆 Aβ 水平)和纵向研究(使用基线血浆 Aβ 水平预测从正常认知向 AD 的转变)进行荟萃分析。对 Medline 和 EMBASE 数据库进行了搜索,生成了相关研究的初始列表,并选择了作者来获取更多数据。十二项横断面研究(n = 1483)和七项纵向研究(n = 3920)符合荟萃分析的纳入标准。 Review Manager 4.2 版使用随机效应模型计算加权平均差 (WMD)。在纵向研究中,转变为 AD 的认知正常个体具有较高的基线 Aβ1-40 和 Aβ1-42 水平(分别为 WMD:10.29,z = 3.80,p = 0.0001 和 WMD:8.01,z = 2.76,p = 0.006),并且 Aβ1-42/Aβ1-40 比率无显着增加(WMD: 0.03,z = 1.65,p = 0.10)。在横断面研究中,与认知正常个体相比,AD 患者的 Aβ1-42 水平略有降低(WMD:−2.84,z = 1.73,p = 0.08),但 Aβ1-40 水平没有显着差异(WMD:3.43,z = 0.40,p = 0.69)。我们的系统综述提出了一个模型,该模型显示认知稳定的个体与继续发展为 AD 痴呆的个体血浆 Aβ 水平的差异纵向变化。认知正常老年人中的基线 Aβ1-40 和 Aβ1-42 水平可能是 AD 进展率较高的预测因素,应作为潜在的生物标志物进行进一步探索。
Plasma amyloid-β (Aβ) levels have been proposed as biomarkers of Alzheimer’s disease (AD), but studies have produced inconsistent results. We present a meta-analytic review of cross-sectional studies that examined plasma Aβ levels in AD and cognitively normal subjects, and longitudinal studies that used baseline plasma Aβ levels to predict conversion from normal cognition to AD. Medline and EMBASE databases were searched to generate an initial list of relevant studies, and selected authors approached for additional data. Twelve cross- sectional studies (n = 1483) and seven longitudinal (n = 3920) met the inclusion criteria for meta-analysis. Random effects model was used to calculate the weighted mean difference (WMD) by Review Manager Version 4.2. In longitudinal studies, cognitively normal individuals who converted to AD had higher baseline Aβ1-40 and Aβ1-42 levels (WMD: 10.29, z = 3.80, p = 0.0001 and WMD: 8.01, z = 2.76, p = 0.006, respectively), and non-significantly increased Aβ1-42/Aβ1-40 ratio (WMD: 0.03, z = 1.65, p = 0.10). In cross sectional studies, compared to cognitively normal individuals, AD patients had marginally but non-significantly lower Aβ1-42 levels (WMD:−2.84, z = 1.73, p = 0.08), but Aβ1-40 levels were not significantly different (WMD: 3.43, z = 0.40, p = 0.69). Our systematic review suggests a model of differential longitudinal changes in plasma Aβ levels in cognitively stable individuals versus those who go on to develop AD dementia. Baseline Aβ1-40 and Aβ1-42 levels in cognitively normal elderly individuals might be predictors of higher rates of progression to AD, and should be further explored as potential biomarkers.