Turner Arlener D, Locklear Clarence E, Oruru Daisha, Briggs Anthony Q, Bubu Omonigho M, Seixas Azizi
Center for Translational Sleep and Circadian Sciences, Department of Psychiatry & Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL, United States.
Department of Neurology, Grossman School of Medicine, New York University, New York, NY, United States.
Front Aging Neurosci. 2023 Jan 4;14:1017521. doi: 10.3389/fnagi.2022.1017521. eCollection 2022.
We determined the interactive associations of apolipoprotein e4 (APOE-e4), and obstructive sleep apnea (OSA) on biomarkers of Alzheimer's disease and examined for racial/ethnic differences of this association.
We used data from the National Alzheimer's Coordinating Center Uniform Dataset (NACC UDS). All participants undergo annual observations, including demographic survey, battery of neuropsychological tests, blood draw (with genotyping), and a clinical evaluation with medical and cognitive/dementia status assessment, while a subset of participants have cerebrospinal fluid (CSF) biomarkers and neuroimaging data. Biomarkers of AD were characterized as the presence of abnormally low amyloid in CSF, validated Aβ cut off protocols, and total segmented hippocampal volume, and volume of white matter hyper intensities (WMH). While clinical markers (to preview cognitive relationships) were characterized the Montreal Cognitive Assessment (MOCA).
Biomarker and clinical marker data were derived from 1,387 participants at baseline (mean age = 69.73 ± 8.32; 58.6% female; 13.7% Black/African American), 18.4% of the sample had sleep apnea, and 37.9% were APOE-e4 carriers. Our results confirmed previous reports that OSA and APOE-e4 were independently associated with AD through abnormal levels of amyloid ( = 4.27; = 0.040; = 60.88; < 0.000, respectively), WMH volume ( = 4.27; = 0.040; = 60.88; < 0.000, respectively), and MOCA scores ( = 4.27; = 0.040; = 60.88; < 0.000, respectively). No significant interaction between OSA and APOE-e4 relative to amyloid emerged, however, race stratified analyses indicated the interaction of OSA and APOE-e4 and was significantly associated with WMH and hippocampal volume in Black/African American, but not white participants.
OSA and APOE-e4 are interactively associated with WHM in Black/African Americans. This interaction may partially explicate increased levels of risk in this population.
我们确定了载脂蛋白E4(APOE-e4)与阻塞性睡眠呼吸暂停(OSA)在阿尔茨海默病生物标志物方面的交互作用,并研究了这种关联的种族/民族差异。
我们使用了来自国家阿尔茨海默病协调中心统一数据集(NACC UDS)的数据。所有参与者每年接受观察,包括人口统计学调查、一系列神经心理学测试、采血(进行基因分型)以及对医疗和认知/痴呆状态进行评估的临床评估,而一部分参与者有脑脊液(CSF)生物标志物和神经影像学数据。AD的生物标志物特征为脑脊液中淀粉样蛋白异常低水平的存在、经过验证的Aβ截断方案、海马总体积分段以及白质高信号(WMH)体积。而临床标志物(以预测认知关系)特征为蒙特利尔认知评估(MOCA)。
生物标志物和临床标志物数据来自1387名基线参与者(平均年龄=69.73±8.32;58.6%为女性;13.7%为黑人/非裔美国人),18.4%的样本有睡眠呼吸暂停,37.9%是APOE-e4携带者。我们的结果证实了先前的报告,即OSA和APOE-e4通过淀粉样蛋白异常水平(分别为=4.27;=0.040;=60.88;<0.000)、WMH体积(分别为=4.27;=0.040;=60.88;<0.000)和MOCA评分(分别为=4.27;=0.040;=60.88;<0.000)与AD独立相关。然而,相对于淀粉样蛋白,OSA和APOE-e4之间未出现显著交互作用,不过种族分层分析表明OSA和APOE-e4的交互作用与黑人/非裔美国人的WMH和海马体积显著相关,而在白人参与者中则不然。
在黑人/非裔美国人中,OSA和APOE-e4与WMH存在交互关联。这种交互作用可能部分解释了该人群中风险水平的升高。