Serum amyloid-beta levels are increased in patients with obstructive sleep apnea syndrome.

Serum amyloid-beta levels are increased in patients with obstructive sleep apnea syndrome.
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DOI:
10.1038/srep13917
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发表时间:
2015-09-09
期刊:
影响因子:
4.6
通讯作者:
Wang YJ
Wang YJ
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bu XL;Liu YH;Wang QH;Jiao SS;Zeng F;Yao XQ;Gao D;Chen JC;Wang YJ

文献摘要

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淀粉样蛋白- β (Aβ)与缺氧之间的关键联系已在体外和动物研究中得到证实,但尚未在人体中得到证实。阻塞性睡眠呼吸暂停综合征(OSAS)是一种以夜间间歇性低氧血症为特征的常见疾病。本研究旨在探讨OSAS患者慢性间歇性缺氧与Aβ之间的关系。本研究包括45名认知正常的OSAS患者和49名年龄和性别匹配的诊断为单纯性打鼾而非OSAS的受试者。采用ELISA试剂盒检测血清Aβ40、Aβ42、总tau蛋白和磷酸化tau 181 (P-tau 181)水平。所有受试者均采用夜间多导睡眠仪和认知测试进行评估。与对照组相比,OSAS患者血清中Aβ40、Aβ42和总Aβ水平均显著升高,且这些水平均与呼吸暂停低通气指数、氧去饱和指数、氧合血红蛋白平均和最低饱和度呈正相关。此外,OSAS患者血清P-tau 181水平显著升高,且这些水平与血清Aβ水平呈正相关。本研究提示慢性间歇性缺氧与Aβ水平升高之间存在关联,提示缺氧可能与阿尔茨海默病的发病机制有关。
A critical link between amyloid-beta (Aβ) and hypoxia has been demonstrated in in vitro and animal studies but has not yet been proven in humans. Obstructive sleep apnea syndrome (OSAS) is a common disorder that is characterized by nocturnal intermittent hypoxaemia. This study sought to examine the association between the chronic intermittent hypoxia and Aβ in OSAS patients. Forty-five cognitively normal OSAS patients and forty-nine age- and gender-matched subjects diagnosed with simple snoring and not OSAS were included in the present study. Serum Aβ40, Aβ42, total tau and phosphorylated tau 181 (P-tau 181) levels were measured using ELISA kits. All subjects were evaluated with nighttime polysomnography and cognitive tests. Compared with the controls, the OSAS patients exhibited significantly higher serum Aβ40, Aβ42 and total Aβ levels, and each of these levels was positively correlated with the apnea-hypopnea index, the oxygen desaturation index, and the mean and lowest oxyhaemoglobin saturations in the OSAS patients. Moreover, the OSAS patients exhibited strikingly higher serum P-tau 181 levels, and these levels were positively correlated with serum Aβ levels. This study suggests that there is an association between chronic intermittent hypoxia and increased Aβ levels, implying that hypoxia may contribute to the pathogenesis of Alzheimer’s disease.