Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later
Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later
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DOI：
10.1212/wnl.0b013e3182918ca6
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发表时间：
2013-05-01
期刊：
影响因子：
9.9
通讯作者：
Morris, John C.
中科院分区：
文献类型：
--
作者：
Roe, Catherine M.;Fagan, Anne M.;Morris, John C.
目的：我们比较了阿尔茨海默病（AD）分子生物标志物的能力，包括淀粉样蛋白成像和CSF生物标志物（A β（42），tau，ptau（181），tau/A β（42），ptau（181）/A β（42）），以预测45 - 88岁认知正常成年人发生认知障碍的时间，并随访长达7.5年。使用了来自Knight阿尔茨海默病研究中心参与者（N = 201）的纵向数据，平均随访3.70年（SD = 1.46年）。在临床评估后1年内进行淀粉样蛋白成像和CSF采集表明认知正常的参与者有资格参加。考克斯比例风险模型测试了个体生物标志物是否与发生认知障碍的时间相关。使用生物标志物和参与者人口统计学变量开发了“扩展”模型。模型的预测值进行了compared.Results：所有生物标志物的异常水平与更快的时间认知障碍，和一些参与者与异常的生物标志物水平保持认知正常长达6.6年。在单个生物标志物之间没有发现预测值的差异（p > 0.074），我们也没有发现扩展的生物标志物模型之间的差异（p > 0.312）。每个扩展的模型比仅包含生物标志物的模型更好地预测偶发性认知损害（p < 0.005）。结论：我们的结果表明，这里研究的所有AD生物标志物预测偶发性认知损害，并支持生物标志物在痴呆症状出现前至少几年发出潜在AD病理信号的假设。神经病学（R）201380：1784-1791
Objectives: We compared the ability of molecular biomarkers for Alzheimer disease (AD), including amyloid imaging and CSF biomarkers (A beta(42), tau, ptau(181), tau/A beta(42), ptau(181)/A beta(42)), to predict time to incident cognitive impairment among cognitively normal adults aged 45 to 88 years and followed for up to 7.5 years.Methods: Longitudinal data from Knight Alzheimer's Disease Research Center participants (N = 201) followed for a mean of 3.70 years (SD = 1.46 years) were used. Participants with amyloid imaging and CSF collection within 1 year of a clinical assessment indicating normal cognition were eligible. Cox proportional hazards models tested whether the individual biomarkers were related to time to incident cognitive impairment. "Expanded" models were developed using the biomarkers and participant demographic variables. The predictive values of the models were compared.Results: Abnormal levels of all biomarkers were associated with faster time to cognitive impairment, and some participants with abnormal biomarker levels remained cognitively normal for up to 6.6 years. No differences in predictive value were found between the individual biomarkers (p > 0.074), nor did we find differences between the expanded biomarker models (p > 0.312). Each expanded model better predicted incident cognitive impairment than the model containing the biomarker alone (p < 0.005).Conclusions: Our results indicate that all AD biomarkers studied here predicted incident cognitive impairment, and support the hypothesis that biomarkers signal underlying AD pathology at least several years before the appearance of dementia symptoms. Neurology (R) 201380:1784-1791