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首页> 外文期刊>Journal of Alzheimer's disease: JAD >Does Caffeine Consumption Modify Cerebrospinal Fluid Amyloid-beta Levels in Patients with Alzheimer's Disease?
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Does Caffeine Consumption Modify Cerebrospinal Fluid Amyloid-beta Levels in Patients with Alzheimer's Disease?

机译：咖啡因消耗会改变阿尔茨海默氏病患者的脑脊液淀粉样蛋白水平吗？

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Caffeine may be protective against Alzheimer's disease (AD) by modulating amyloid-beta (A beta) metabolic pathways. The present work aimed to study a possible association of caffeine consumption with the cerebrospinal fluid (CSF) biomarkers, particularly A beta. The study included 88 patients with AD or mild cognitive impairment. The consumption of caffeine and theobromine was evaluated using a validated food questionnaire. Quantification of caffeine and main active metabolites was performed with liquid chromatography coupled to tandem mass spectrometry. The levels of A beta(1-42), total tau, and phosphorylated tau in the CSF were determined using sandwich ELISA methods and other A beta species, A beta(X-38), A beta(X-40), and A beta(X-42), with the MSD A beta Triplex assay. The concentration of caffeine was 0.79 +/- 1.15 mu g/mL in the CSF and 1.20 +/- 1.88 mu g/mL in the plasma. No correlation was found between caffeine consumption and A beta(42) in the CSF. However, a significant positive correlation was found between the concentrations of theobromine, both in the CSF and in the plasma, with A beta(42) in the CSF. Theobromine in the CSF was positively correlated with the levels of other xanthines in the CSF, but not in the plasma, suggesting that it may be formed by central metabolic pathways. In conclusion, caffeine consumption does not modify the levels of CSF biomarkers, and does not require to be controlled for when measuring CSF biomarkers in a clinical setting. Since theobromine is associated with a favorable A beta profile in the CSF, the possibility that it might have a protective role in AD should be further investigated.
机译：咖啡因可能通过调节淀粉样β（A beta）代谢途径来预防阿尔茨海默氏病（AD）。本工作旨在研究咖啡因摄入与脑脊液（CSF）生物标志物，尤其是A beta的可能联系。该研究纳入了88名患有AD或轻度认知障碍的患者。使用经过验证的食物问卷评估咖啡因和可可碱的消耗量。咖啡因和主要活性代谢物的定量是通过液相色谱与串联质谱联用进行的。使用夹心ELISA方法和其他A beta种类，A beta（X-38），A beta（X-40）和A确定ASF（1-42），总tau和磷酸化tau的水平beta（X-42），采用MSD A beta三重分析法。咖啡因的浓度在CSF中为0.79 +/- 1.15μg / mL，在血浆中为1.20 +/- 1.88μg / mL。在咖啡因中，咖啡因的摄入与A beta（42）之间没有相关性。但是，在脑脊液和血浆中可可碱的浓度与脑脊液中的A beta（42）之间发现显着正相关。脑脊液中的可可碱与脑脊液中其他黄嘌呤的水平呈正相关，但与血浆中的黄嘌呤却无正相关，这表明它可能是由中央代谢途径形成的。总之，摄入咖啡因不会改变CSF生物标志物的水平，并且在临床环境中测量CSF生物标志物时不需要控制咖啡因。由于可可碱与脑脊液中有利的Aβ谱有关，因此应进一步研究其可能在AD中起保护作用的可能性。

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