Kheirandish-Gozal Leila, Philby Mona F, Alonso-Álvarez María Luz, Terán-Santos Joaquin, Gozal David
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Chicago, IL.
Sleep Unit, CIBER of Respiratory Diseases, Instituto Carlos III, CIBERES, Hospital Universitario de Burgos (HUBU), Burgos, Spain.
Sleep. 2016 Jun 1;39(6):1225-32. doi: 10.5665/sleep.5838.
Obese children are at increased risk for developing obstructive sleep apnea (OSA), and both of these conditions are associated with an increased risk for end-organ morbidities. Both OSA and obesity (OB) have been associated with increased risk for Alzheimer disease (AD). This study aimed to assess whether OSA and OB lead to increased plasma levels of 2 AD markers amyloid β protein 42 (Aβ42) and pre-senilin 1 (PS1).
Fasting morning plasma samples from otherwise healthy children with a diagnosis of OB, OSA, or both (OSA+OB), and controls, and in a subset of children with OSA after adenotonsillectomy (T&A) were assayed for Aβ42 and PS1 levels using commercial enzyme-linked immunosorbent assay kits.
286 children (mean age of 7.2 ± 2.7 y) were evaluated. Compared to control subjects, OB children had similar Aβ42 (108.3 ± 31.7 pg/mL versus 83.6 ± 14.6 pg/mL) and PS1 levels (0.89 ± 0.44 ng/mL versus 0.80 ± 0.29 pg/mL). However, OSA children (Aβ42: 186.2 ± 66.7 pg/mL; P < 0.001; PS1: 3.42 ± 1.46 ng/mL; P < 0.001), and particularly OSA+OB children had significant elevations in both Aβ42 (349.4 ± 112.9 pg/mL; P < 0.001) and PS1 (PS1: 4.54 ± 1.16 ng/mL; P < 0.001) circulating concentrations. In a subset of 24 children, T&A resulted in significant reductions of Aβ42 (352.0 ± 145.2 versus 151.9 ± 81.4 pg/mL; P < 0.0001) and PS1 (4.82 ± 1.09 versus 2.02 ± 1.18 ng/mL; P < 0.0001).
Thus, OSA, and particularly OSA+OB, are associated with increased plasma levels of AD biomarkers, which decline upon treatment of OSA in a representative, yet not all- encompassing subset of patients, suggesting that OSA may accelerate AD-related processes even in early childhood. However, the cognitive and overall health-related implications of these findings remain to be defined.
肥胖儿童患阻塞性睡眠呼吸暂停（OSA）的风险增加，而这两种情况都与终末器官发病风险增加有关。OSA和肥胖（OB）都与阿尔茨海默病（AD）风险增加有关。本研究旨在评估OSA和OB是否会导致血浆中两种AD标志物淀粉样β蛋白42（Aβ42）和早老素1（PS1）水平升高。
使用商用酶联免疫吸附测定试剂盒，对诊断为OB、OSA或两者兼有（OSA+OB）的健康儿童以及对照组儿童的空腹晨间血浆样本，以及部分接受腺样体扁桃体切除术（T&A）后的OSA儿童亚组样本进行Aβ42和PS1水平检测。
共评估了286名儿童（平均年龄7.2±2.7岁）。与对照组相比，OB儿童的Aβ42（分别为108.3±31.7 pg/mL和83.6±14.6 pg/mL）和PS1水平（分别为0.89±0.44 ng/mL和0.80±0.29 pg/mL）相似。然而，OSA儿童（Aβ42：186.2±66.7 pg/mL；P<0.001；PS1：3.42±1.46 ng/mL；P<0.001），尤其是OSA+OB儿童的循环Aβ42（349.4±112.9 pg/mL；P<0.001）和PS1（PS1：4.54±1.16 ng/mL；P<0.001）浓度显著升高。在24名儿童的亚组中，T&A导致Aβ42（分别为352.0±145.2和151.9±81.4 pg/mL；P<0.0001）和PS1（4.82±1.09和2.02±1.18 ng/mL；P<0.0001）显著降低。
因此，OSA，尤其是OSA+OB，与AD生物标志物的血浆水平升高有关，在一个具有代表性但并非涵盖所有患者的亚组中，OSA治疗后这些标志物水平下降，这表明OSA可能即使在儿童早期也会加速AD相关进程。然而，这些发现对认知和整体健康的影响仍有待确定。
