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Amyloid Burden in Obstructive Sleep Apnea.

Authors :
Chang-Ho Yun
Ho-Young Lee
Seung Ku Lee
Hyun Kim
Hyung Suk Seo
Seong Ae Bang
Sang Eun Kim
Greve, Douglas N.
Au, Rhoda
Chol Shin
Thomas, Robert J.
Yun, Chang-Ho
Lee, Ho-Young
Lee, Seung Ku
Kim, Hyun
Seo, Hyung Suk
Bang, Seong Ae
Kim, Sang Eun
Shin, Chol
Source :
Journal of Alzheimer's Disease; 2017, Vol. 59 Issue 1, p21-29, 9p, 1 Black and White Photograph, 1 Chart, 1 Graph
Publication Year :
2017

Abstract

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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13872877
Volume :
59
Issue :
1
Database :
Complementary Index
Journal :
Journal of Alzheimer's Disease
Publication Type :
Academic Journal
Accession number :
124021353
Full Text :
https://doi.org/10.3233/JAD-161047