Associations between risk of Alzheimer's disease and obstructive sleep apnea, intermittent hypoxia, and arousal responses: A pilot study

Abstract

ObjectivesObstructive sleep apnea (OSA) may increase the risk of Alzheimer's disease (AD). However, potential associations among sleep-disordered breathing, hypoxia, and OSA-induced arousal responses should be investigated. This study determined differences in sleep parameters and investigated the relationship between such parameters and the risk of AD.MethodsPatients with suspected OSA were recruited and underwent in-lab polysomnography (PSG). Subsequently, blood samples were collected from participants. Patients' plasma levels of total tau (T-Tau) and amyloid beta-peptide 42 (Aβ42) were measured using an ultrasensitive immunomagnetic reduction assay. Next, the participants were categorized into low- and high-risk groups on the basis of the computed product (Aβ42 × T-Tau, the cutoff for AD risk). PSG parameters were analyzed and compared.ResultsWe included 36 patients in this study, of whom 18 and 18 were assigned to the low- and high-risk groups, respectively. The average apnea–hypopnea index (AHI), apnea, hypopnea index [during rapid eye movement (REM) and non-REM (NREM) sleep], and oxygen desaturation index (≥3%, ODI-3%) values of the high-risk group were significantly higher than those of the low-risk group. Similarly, the mean arousal index and respiratory arousal index (R-ArI) of the high-risk group were significantly higher than those of the low-risk group. Sleep-disordered breathing indices, oxygen desaturation, and arousal responses were significantly associated with an increased risk of AD. Positive associations were observed among the AHI, ODI-3%, R-ArI, and computed product.ConclusionsRecurrent sleep-disordered breathing, intermittent hypoxia, and arousal responses, including those occurring during the NREM stage, were associated with AD risk. However, a longitudinal study should be conducted to investigate the causal relationships among these factors.

The relationship between obstructive sleep apnea and circulating tau levels: A meta‐analysis

“…Sixty‐seven papers were further excluded after screening titles and abstracts, leaving 10 citations for full‐text review. Three papers were subsequently excluded for the following reasons: One study defined OSA using a questionnaire (Huang et al., 2021 ); another study divided patients into normal‐to‐moderate and severe OSA groups (Tsai, Liu, et al., 2022 ); one study did not group by OSA severity (Tsai, Wu, et al., 2022 ). At last, seven papers were considered eligible for the meta‐analysis.…”

“…A PRISMA flow diagram of the study selection process is presented in ( Tsai, Wu, et al, 2022). At last, seven papers were considered eligible for the meta-analysis.…”

Continuous Positive Airway Pressure Reduces Plasma Neurochemical Levels in Patients with OSA: A Pilot Study

“…A related study reported a significant association between a high mean AHI and increased neurochemical biomarker levels in patients with OSA without dementia [ 29 ]. Another study analyzed PSG parameters and neurochemical biomarker levels and suggested that the elevated AHI, ODI-3%, and arousal indexes were significantly associated with the risk of AD [ 30 ]. OSA acts in synergism with neurochemical biomarkers (i.e., Aβ 42 and T-tau), and patients with mild cognitive impairment having untreated OSA may have shorter progression time to AD compared with those with only mild cognitive impairment [ 31 ].…”

Association of Low Arousal Threshold Obstructive Sleep Apnea Manifestations with Body Fat and Water Distribution

“…These traits interact with each other and contribute to the periodic repetition of respiratory or frequent arousal events in patients with OSA. Recent studies have demonstrated that one of the endophenotypic traits, namely low-ArTH OSA, which may contribute to the highly frequent arousal response, may be associated with or even aggravate other related diseases (e.g., periodic limb movements, cognitive impairment, Alzheimer’s disease) [ 28 , 29 , 30 ]. Therefore, understanding the mechanisms underlying these endophenotypic OSA traits could help to prevent the disease presentation or allow for precise OSA treatment based on the specific pathophysiological condition of each individual.…”