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阿尔茨海默病中性粒细胞与淋巴细胞比值的评估。

The evaluation of neutrophil-lymphocyte ratio in Alzheimer's disease.

机构信息

Department of Internal Medicine, Division of Geriatric Medicine, Hacettepe University, Faculty of Medicine, Ankara, Turkey.

出版信息

Dement Geriatr Cogn Disord. 2012;34(2):69-74. doi: 10.1159/000341583. Epub 2012 Aug 23.

Abstract

BACKGROUND/AIM: There is growing consensus in the literature that inflammation plays a significant role in the pathophysiology of Alzheimer's disease (AD). The blood neutrophil-lymphocyte ratio (NLR) is a new, inexpensive and easily applicable marker of inflammation. The aim of this study was to investigate the association between NLR, as an inflammatory biomarker, and AD.

METHODS

241 AD patients and 175 patients with normal cognitive function were evaluated in this study.

RESULTS

The mean ± SD NLR of AD patients was significantly higher than that of patients with normal cognitive function (3.21 ± 1.35 vs. 2.07 ± 0.74, p < 0.001, respectively). Receiver operating characteristic curve analysis suggested that the optimum NLR cutoff point for AD was 2.48 with 69.29% sensitivity, 79.43% specificity, 82.30% positive predictive values and 65.30% negative predictive values. Logistic regression analysis showed that elevated NLR (OR: 4.774, 95% CI: 2.821-8.076, p < 0.001) was an independent variable for predicting AD.

CONCLUSION

Elderly people with AD have higher NLR than healthy controls. Elevated NLR levels are usually considered as an inflammatory marker. The results of this study suggested that inflammation plays a role in the pathogenesis of AD.

摘要

背景/目的:越来越多的文献认为炎症在阿尔茨海默病(AD)的病理生理学中起着重要作用。中性粒细胞与淋巴细胞比值(NLR)是一种新的、廉价且易于应用的炎症标志物。本研究旨在探讨 NLR(一种炎症生物标志物)与 AD 之间的关系。

方法

本研究评估了 241 例 AD 患者和 175 例认知功能正常的患者。

结果

AD 患者的 NLR 平均值±标准差明显高于认知功能正常的患者(3.21±1.35 比 2.07±0.74,p<0.001)。受试者工作特征曲线分析表明,AD 的最佳 NLR 截断点为 2.48,具有 69.29%的敏感性、79.43%的特异性、82.30%的阳性预测值和 65.30%的阴性预测值。Logistic 回归分析表明,升高的 NLR(OR:4.774,95%CI:2.821-8.076,p<0.001)是预测 AD 的独立变量。

结论

患有 AD 的老年人的 NLR 高于健康对照组。升高的 NLR 水平通常被认为是一种炎症标志物。本研究结果表明,炎症在 AD 的发病机制中起作用。

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