Plasma Amiloid β42 in Patients with Obstructive Sleep Apnea before and after CPAP-Therapy: Pilot Study

Abstract

The aim of this pilot research was to assess the sleep fragmentation influence on amyloid β42 (Aβ42) plasma levels before and after СPAP in patients with obstructive sleep apnea (OSA). Materials and Methods: The study involved 24 patients (mean age of 52.5±2.7 years) with OSA and 20 persons without OSA (mean age of 49.1±8.2 years). All participants underwent overnight polysomnography, The Aβ42 level was determined in blood plasma by an immunoassay method. Patients with OSA were treated with auto-CPAP for 3 months. Results: The research showed the following results in patients with OSA before CPAP, as compared to control: sleep fragmentation 1-2 times, increases in non-rapid eye movement sleep stage by 60% (P<0.05) and arousal index by 55% (P<0.05), and decreases in slow-wave sleep duration by 40% (P<0.05) and rapid-eye-movement sleep by 43% (P<0.05). After CPAPtherapy, a decrease in arousal index by 40% (P<0.05) and apnea/hypopnea index (P<0.05), and increases in oxygen saturation by 17% (P<0.05), the slow-wave sleep duration by 56% (P<0.05) and rapid-eye-movement sleep by 55% (P<0.05) were found. Aβ42 levels were significantly lower in the group with OSA before CPAP-therapy, as compared to the control group and the group with OSA after CPAP-therapy (P<0.05). There were no differences in Aβ42 levels after treatment between control and main group. Conclusion: Moderate and severe OSA is associated with a decrease in Aβ42 plasma level. CPAP-therapy leads to increase this peptide in blood plasma.

Positive airway pressure improves amnestic mild cognitive impairment in patients diagnosed with obstructive sleep apnoea hypopnoea syndrome. A review of the evidence

“…The importance of sleep for optimal function of the glymphatic system has been previously reported in humans [23,[28][29][30][31][32]34].…”

“…In the long-term this inflammatory process leads to neuronal death causing structural changes in the brain [37,58]. Deficits in synaptic plasticity and neuronal death leads to cognitive impairment [11,29,31,35].…”

“…Search term PubMed ("Mild cognitive impairment" OR "cognitive decline" OR "cognitive dysfunction" OR "mild cognitive deficit" OR "Alzheimer disease" OR AD OR amyloid OR "MCI" OR "amnestic mild cognitive impairment" OR "degenerative disease" OR "amyloid precursor protein A total of 45 studies were found. Of the 45, 15 studies discussed the hypothesised glymphatic system in relation to sleep [11,12,[23][24][25][26][27][28][29][30][31][32][33][34][35], 5 studies assessed the impact of PAP on brain fluid diffusivity in patients with OSAHS [36][37][38][39][40], 4 studies assessed the influence of PAP treatment on the level of AD biomarkers [29,31,41,42], 11 studies measured the impact of PAP treatment on cognitive function in OSAHS [1,4,14,[43][44][45][46][47][48][49][50] and 10 studies measured the impact of PAP treatment on cognitive function in OSAHS and aMCI/AD [7,8,17,20,21,[51][52][53][54]…”

“…It has been hypothesised that the glymphatic system is most effective during slow wave sleep; with the purpose of CSF influx into the brain, mixing with the interstitial fluid containing the metabolic waste such as amyloid beta (Aβ), which accumulates during wakefulness. The combined fluid containing the proteins are washed out of the parenchyma into the CSF and the blood stream via the blood brain barrier, for elimination through the kidneys and liver [23,28,30,31,34,56].…”

“…It has been suggested that tau is a product of axonal loss mainly due to increase in hyperphosphorylated tau which cannot bind to the microtubules of the axon. Therefore, support from tau is no longer available causing axon instability and neuronal death leading to neurodegeneration (Figure 1a) [11,29,31,35,57,58]. This is likely to be caused by intermittent hypoxia leading to inflammation in the brain (Figure 1a).…”