Table 2.
Biomarkers results in patients with obstructive sleep apnea syndrome and Alzheimer’s disease
| Reference | Sample | Method | Results |
|---|---|---|---|
| Lee et al. (48) | n=727 SDB,n=3635 non-SDB | Cohort stud via propensity score matching | SDB group more likely to develop AD after matching and adjusting for other risk factors |
| Gaeta et al. (49) | n=116/128 mild-moderate AD were diagnosed with OSAS | PSG for assessing the severity of OSAS and Mini-Mental State Examination + EES + APOE status for AD severity | The prevalence of APOE ε4 was not significantly different between patients with and without severe OSA |
| Przybylska-Kud et al. (50) | n=31 C, n=38 mild-moderate OSAS, n=43 severe OSAS | Aβ 1–40 and Aβ 1–42 plasma concentrations | OSAseveredemonstrated higher concentrations of Aβ 1–40 compared with the rest groups |
| Gonzalez Vicente et al. (51) | Rats | Under intracerebro-ventricular streptozotocin, a drug that has been described to cause Alzheimer-like behavioral and histopathological impairments | ↑ sensitivity to CO<sub>2</sub> during wakefulness, ↑ Aβ in the Locus Coeruleus, no change in tau protein phosphorylation and sleep disruption |
| Mendes et al. (52) | n=318 AD | assessed for multimorbidity and neuroimaging biomarkers | OSA was associated with lower amyloid-PET SUV ratios |
| Lutsey et al. (23) | n=1667 | OSAS and risk for dementia | Sleeping <7 versus8-≤9 hours, also correlated significantly with a higher risk of dementia and AD |
| Kahya et al. (53) | n=36 [APOE ε4 carriers (n=9), non- carriers (n=27)] cognitively normal older adults without self-reported sleep apnea | Actigraph + PSQI + ESS | Cognitively normal older APOE ε4 carriers without self-reported sleep apnea had disrupted sleep compared to non-carriers |
| Ju et al. (54) | n=10 OSA, n=31 C | PSG and lumbar puncture for CSF biomarkers | SWA is decreased in moderate-to-severe OSA and neuronally derived proteins, but not total protein, were also decreased in the OSA group |
| Lutsey et al. (24) | n=312 | PSG and MRI twice. They were stratified according to the sleep duration (<7 hours, 7-to-<8 hours and ≥8 hours) | No significant statistical relationship between OSAS and short sleep with cerebral markers of vascular dementia and Alzheimer’s disease |
| Bu et al. (55) | n=45 OSAS, n=49 C | The cognitively normal OSAS patients exhibited significantly higher serum Aβ40, Aβ42 and total Aβ levels, and each of these levels were positively correlated with the severity of OSAS and the extent of hypoxia. In OSAS patients, the serum P-tau 181 levels were higher and correlated with the Aβ levels | ↑ Aβ levels in the serum are correlated with the severity of chronic intermittent hypoxia in OSAS patients and may contribute to the pathogenesis of AD |
| Buratti et al. (25) | n=162 AD, n= 69 C, n=93 OSAS | U/S of external and internal arteries | Common lesions of external and internal cranial arteries as well as that the extent of cerebrovascular damage was correlated with the severity of OSAS |
| Osorio et al. (56) | n=19 severe SDB,n=51 mild, n=25 normal elderly cognitive normal | SDB severity, CSF measures of phosphorylated-tau (P-Tau), total-tau (T- Tau), and amyloid beta 42 (Aβ42), as well as ApoE allele status | SDB in ApoE3+ and ApoE2+ normal elderly is associated with changes in specific biomarkers of Late onset Alzheimer’s disease |
| Nikodemova et al. (57) | n=755 adults evaluated for their sleep characteristics | PSG + APOE4 + neurocognitive test battery | The combination of moderate to severe SDB and APOE4 genotype is associated with poorer performance on some neurocognitive tests with memory and executive function components |
| Shiota et al. (58) | Mice triple transgenic AD | Were evaluated Aβ profile, cognitive brain function, and brain pathology. | CIH directly increased levels of Aβ42 in the AD model (but not Aβ40 and HIF-1↑), no significant changes in cognitive function. Therefore, OSA may aggravate AD |
| Kaushal et al. (59) | Murine models (adult male human ApoE4-targeted replacement mice (hApoE4) and wild-type (WT) controls) | Sleep disorder such as sleep apnea (i.e., IH, SF, or both) would lead to a more pronounced disruption of sleep integrity in a murine model of AD | IH, SF and IH+SF, are sufficient to elicit sleep deficits, excessive sleepiness, and hApoE4 exacerbates such effects |
Note: AD = Alzheimer’s disease, Aβ = amyloid-beta, C = control, CSF = cerebrospinal fluid, ESS = Epworth sleep scale, IH = intermittent hypoxia, MRI = magnetic resonance imaging, PET = positron emission tomography, PSG = polysomnography study, PSQI = Pittsburg sleep quality index, SDB = sleep-disorders breathing, SF = sleep fragmentation, SWA = slow wave activity during sleep.