Yun Chang-Ho, Lee Ho-Young, Lee Seung Ku, Kim Hyun, Seo Hyung Suk, Bang Seong Ae, Kim Sang Eun, Greve Douglas N, Au Rhoda, Shin Chol, Thomas Robert J
Department of Neurology, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Department of Nuclear Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
J Alzheimers Dis. 2017;59(1):21-29. doi: 10.3233/JAD-161047.
To test the hypothesis that excessive amyloid deposition is a biological link between obstructive sleep apnea (OSA) and Alzheimer's disease, we determined whether OSA increases cerebral amyloid burden, relative to controls, using Pittsburgh Compound B (PiB) PET imaging. The subjects were adult participants (age 50-65 years) from the Korean Genome and Epidemiology Study. Polysomnography, brain MRI including 3D images, and a detailed neuro-cognitive function test battery were done in 2011-2012. Nineteen OSA subjects (Apnea-Hypopnea Index [AHI] ≥15/h, 21.2±5.1/h; age 58.5±4.1 years; 9 male) and 19 controls (AHI 1.8±1.3/h; age 58.5±4.2 years; 9 male) underwent 60-min dynamic 11C-PiB PET. All subjects were right-handed with normal cognitive function and brain MRI. Controls were matched by age, gender, education, and APOE genotype. A voxel-wise comparison of PiB-PET images between the two groups was performed after spatial and count normalization with cerebellar gray matter as a reference. Covariates included the status of sleep duration, hypertension, diabetes, body mass index, exercise, depressive mood, smoking, and alcohol drinking. Cortical thickness on 3D MRI was also measured and compared between the two groups. The OSA group showed a higher PiB deposition in the right posterior cingulate gyrus and right temporal cortex (corrected p < 0.05). There was no area of higher uptake in the control compared with OSA. Regional differences in cortical thickness were not significant. The study suggests that OSA accelerates amyloid deposition and may contribute to the development or progression of Alzheimer's disease.
为了验证过量淀粉样蛋白沉积是阻塞性睡眠呼吸暂停（OSA）与阿尔茨海默病之间生物学联系这一假设，我们使用匹兹堡化合物B（PiB）PET成像，确定与对照组相比，OSA是否会增加脑淀粉样蛋白负荷。研究对象为韩国基因组与流行病学研究中的成年参与者（年龄50 - 65岁）。在2011 - 2012年进行了多导睡眠图检查、包括三维图像的脑部MRI以及详细的神经认知功能测试。19名OSA受试者（呼吸暂停低通气指数[AHI]≥15/小时，21.2±5.1/小时；年龄58.5±4.1岁；9名男性）和19名对照组（AHI 1.8±1.3/小时；年龄58.5±4.2岁；9名男性）接受了60分钟的动态11C - PiB PET检查。所有受试者均为右利手，认知功能和脑部MRI正常。对照组在年龄、性别、教育程度和APOE基因型方面进行了匹配。以小脑灰质为参考，在空间和计数归一化后，对两组的PiB - PET图像进行体素水平比较。协变量包括睡眠时间、高血压、糖尿病、体重指数、运动、抑郁情绪、吸烟和饮酒状况。还测量并比较了两组三维MRI上的皮质厚度。OSA组在右侧后扣带回和右侧颞叶皮质显示出更高的PiB沉积（校正p<0.05）。与OSA组相比，对照组没有更高摄取区域。皮质厚度的区域差异不显著。该研究表明，OSA会加速淀粉样蛋白沉积，并可能促进阿尔茨海默病的发生或发展。
