Obstructive sleep apnea (OSA) is considered to impair memory processing and increase the expression of amyloid-β (Aβ) and risk for Alzheimer’s disease (AD). Given the evidence that slow-wave sleep (SWS) is important in both memory and Aβ metabolism, a better understanding of the mechanisms by which OSA impacts memory and risk for AD can stem from evaluating the role of disruption of SWS specifically and, when such disruption occurs through OSA, from evaluating the individual contributions of sleep fragmentation (SF) and intermittent hypoxemia (IH). In this study, we used continuous positive airway pressure (CPAP) withdrawal to recapitulate SWS-specific OSA during polysomnography (PSG), creating conditions of both SF and IH in SWS only. During separate PSGs, we created the conditions of SWS fragmentation but used oxygen to attenuate IH. We studied 24 patients (average age of 55 years, 29% female) with moderate-to-severe OSA [Apnea-Hypopnea Index (AHI); AHI4% > 20/h], who were treated and adherent to CPAP. Participants spent three separate nights in the laboratory under three conditions as follows: (1) consolidated sleep with CPAP held at therapeutic pressure (CPAP); (2) CPAP withdrawn exclusively in SWS (OSASWS) breathing room air; and (3) CPAP withdrawn exclusively in SWS with the addition of oxygen during pressure withdrawal (OSASWS + O2). Multiple measures of SF (e.g., arousal index) and IH (e.g., hypoxic burden), during SWS, were compared according to condition. Arousal index in SWS during CPAP withdrawal was significantly greater compared to CPAP but not significantly different with and without oxygen (CPAP = 1.1/h, OSASWS + O2 = 10.7/h, OSASWS = 10.6/h). However, hypoxic burden during SWS was significantly reduced with oxygen compared to without oxygen [OSASWS + O2 = 23 (%min)/h, OSASWS = 37 (%min)/h]. No significant OSA was observed in non-rapid eye movement (REM) stage 1 (NREM 1), non-REM stage 2 (NREM 2), or REM sleep (e.g., non-SWS) in any condition. The SWS-specific CPAP withdrawal induces OSA with SF and IH. The addition of oxygen during CPAP withdrawal results in SF with significantly less severe hypoxemia during the induced respiratory events in SWS. This model of SWS-specific CPAP withdrawal disrupts SWS with a physiologically relevant stimulus and facilitates the differentiation of SF and IH in OSA.
Introduction K-complexes are hallmarks of sleep stage N2 and are thought to be associated with two distinct roles that serve as either or both, a sleep protective mechanism or a cortical arousal response. K-complexes and their morphological features (number, delta surrounding K complexes, etc.) have been implicated in sustained attention as well as in Alzheimer’s disease wherein a decline in the number of K-complexes appeared to discriminate diseased individuals from healthy controls. Yet, age and sex-related changes in K-complex morphology are not well-known. Methods We analyzed data from the Sleep Heart Health Study (SHHS) to understand age- and sex-related changes in K-complex morphology. The SHHS is a cohort study comprised of 5,804 men and women aged 40 and older aimed at investigating the cardiovascular consequences of sleep-disordered breathing. K-complex (on C3/A2) features were quantified using previously published and validated open-source algorithm (DETOKS; Parekh et. al. J. Neurosci Meth. 2015). Three features of K-complexes were studied: number of K-complexes (density), delta (∆SWAK) and alpha (∆alphaK) surrounding K-complexes. Results Of the 5,804 studies available, 3,909 that had at least 6h of usable EEG were analyzed (mean = 62±11 yrs., range [40-90 yrs.], 53%female). With aging, K-complex density and (rho=-0.1, p<0.0001), ∆SWAK (rho=-0.2, p<0.0001) were inversely associated with age, while ∆alphaK (rho=0.1, p<0.01) was significantly positively associated with age. The inverse association of K-complex density with age was greater in men compared to women (rhomen=-0.3, p<0.0001, rhowomen=-0.1, p<0.01). Women had greater K-complex density compared to men (1.8[1.3-2.4] vs. 1.3[0.9-1.8], median[IQR]; std. mean diff =0.4). The changes in K-complex morphology with age remained significant after controlling for OSA severity. Conclusion Age is associated with decline in K-complex morphology such that K-complex density and delta activity surrounding K-complexes declines whereas alpha activity surrounding K-complexes increases. An age-related decline in delta activity surrounding K-complexes and an increase in alpha activity surrounding K-complexes is consistent with the potential role for these features in either sleep-state maintenance or arousal responsiveness. Whether the decline in K-complex morphology seen here with aging, and its interaction with sex-related differences, is accelerated in neurodegenerative disorders such as AD remains to be tested. Support (If Any) Support: NIH K25HL151912, AASMFoundation BS-233-20
Introduction Systems consolidation is one of the major theories of sleep’s function in memory. Sleep is thought to be important in integrating and distributing hippocampal information to cortical structures such that there is less hippocampal activation, while at the same time increasing striatal activation, upon subsequent experience in the same environment that co-occurs with improved performance. Here we sought to examine the evidence supporting systems consolidation across sleep in spatial navigational memory. Methods 15 subjects (28±5 yrs., 8 female) with no prior videogame experience and no sleep disorders were recruited to undergo spatial navigational memory testing before and after a night of sleep. Spatial navigational memory was tested across two functional MR (fMRI) sessions (approx. 7PM and 8AM) separated by in-lab nocturnal polysomnography (NPSG) measured sleep using a virtual 3D Maze. Each fMRI session consisted of six runs: three maze trials interleaved with three control trials. During maze trials participants were instructed to reach a prespecified goal as quickly as possible, whereas during the control trials, participants were instructed to navigate a Z-shaped corridor with no prespecified goal. fMRI data was analyzed in 2-step procedure using Analysis of Functional Neuroimages (AFNI) software package. To estimate hippocampal activity during fMRI, parameter estimates of the %change in blood-oxygen-level-dependent (BOLD) signal using the contrast maze-control were used as the primary metric. Regions of interest were limited to the bilateral hippocampus, parahippocampal gyrus, caudate, and putamen using the Eickhoff-Zilles macro labels from the MNI-N27 template. Results During in-lab NPSG, participants experienced a total sleep time of 6.1±1.1 hrs (8.7±2.9%stage1, 51.2±7.6%stage2, 21.8±8.5%stage3, 18.1±6%REM). Within subjects, compared to pre-sleep, a significantly lower activation of the bilateral hippocampus and parahippocampal gyrus was observed post-sleep (evening-morning %change=0.26±0.11, p<0.05). Compared to pre-sleep, caudate and putamen activity was not significantly different post-sleep (evening-morning %change=-0.02±0.04,p=0.5). Greater evening hippocampal activity was associated with greater change in maze completion times across sleep (rho=0.54, p=0.04). Conclusion In young healthy adults, a night of uninterrupted sleep supports redistribution of hippocampal contribution toward spatial navigation. Greater initial pre-sleep hippocampal contribution was associated with improved recall of spatial navigational memory after a night of sleep. Support (If Any) NIH R21AG059179, R01AG056682, K25HL151912
Introduction The SARS-COVID-19 pandemic restricted in-lab research activities especially in older individuals who are considered at-risk for severe disease. To continue longitudinal sleep research in this population we sought to test the feasibility of remotely conducting at-home sleep and memory research and to compare two ambulatory polysomnography (PSG) devices for ongoing home sleep testing. Methods 20 older (age=65.6±5.5 years) cognitively normal adults (65% female) who had previously undergone 2 nights in-lab sleep, memory and vigilance testing were delivered equipment for 2 nights at-home, technician-guided remote PSG set-up (1 night each for Somté [EEG: Fp1-M2, Cz-M1] and Sleep Profiler (SP) [EEG: Fp1-Fp2] devices- randomized presentation), and 6 timed trials on a 3D spatial maze navigation memory plus morning psychomotor vigilance testing (PVT). The night-to-night differences for devices and in-lab versus at-home testing environments were compared for sleep macro and EEG microarchitecture using paired Wilcoxon rank sum and t-tests where appropriate. First-night maze completion time (CT) and PVT reaction time and lapses were also compared. Results 19 people completed 2 nights at-home PSG, 18 completed PVT and 9 completed all 6 maze trials. Quality frontal EEG signals were obtained for 16 SP and 11 Somté recordings. There was no significant night to night differences (night 1–night 2) between in-lab and at-home environments for total sleep time (mean difference: in-lab= -0.27 vs at-home = 0.35 hours), wake after sleep onset (WASO) (median difference: in-lab= 3.0 vs at-home = 0.7 %WASO), or slow wave sleep (SWS) (mean difference: in-lab= -0.70 vs at-home = 2.3 %SWS). Relative frontal slow wave activity and spindle density were not significantly different between devices or environments. K-complex density (SP= 1.0 vs Somté =2.7/minNREM2, p=0.004) was significantly reduced with the SP device compared to Somté devices. There were no significant differences for maze CT and PVT measures between in-lab and at-home environments. Conclusion The night-to-night differences in sleep macroarchitecture do not appear to be influenced by environment or device however measures of EEG microstructure such as K-complexes, which are amplitude-dependent, may be underestimated with the Sleep Profiler device due to smaller EEG amplitude from a derivation with short inter-electrode distances. Support (if any) NIH (R01AG056031, R01AG056531, K24)
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