Sleep最新文献

Study objectives: Brain pericytes play a crucial role in neurovascular coupling (NVC), regulating cerebral blood flow (CBF) in response to changes in local neuronal activity. However, their activities during sleep remain less understood. Our objective is to investigate the dynamic changes in pericyte activity and related hemodynamic changes during the sleep-wake cycle.

Methods: Using an in vivo calcium (Ca2+) imaging tool, we recorded cytosolic Ca2+ transient dynamics from brain pericytes across natural sleep-wake cycles in the prefrontal cortex (PFC) and lateral hypothalamus (LH) of mice expressing the Ca2+ sensor GCaMP6f specifically in pericytes. Using an in vivo vascular imaging tool, capillary diameter and red blood cell (RBC) velocity dynamic changes in PFC and LH were recorded and calculated across natural sleep-wake cycles.

Results: Our results show that PFC pericytes exhibit low basal Ca2+ transients during non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS), while showing synchronous Ca2+ peaks following transitions from sleep to waking. In contrast, LH pericytes display diverse Ca2+ transient patterns across the sleep-wake cycle, with 81.3%, 15.6%, and 56.3% presenting Ca2+ peaks during NREMS, REMS, and waking, respectively. Hemodynamic recordings in PFC demonstrated greater fluctuations in RBC velocity during waking compared to NREMS, likely associated with periodic pericyte activations during waking. In LH, average capillary diameter and RBC velocity significantly increased during waking compared to NREMS, aligning with the predominantly NREMS-ON pattern of pericyte Ca2+ transients and frequent capillary stalling observed during NREMS.

Conclusions: Our findings identified the region-specific pericyte activity patterns that may contribute to local CBF dynamics during natural sleep-wake cycles, emphasizing their importance in maintaining neurovascular function in different vigilant states.

Study objectives: Impaired spindle activity and hypoxia have been linked to dementia. However, their joint mechanism remains unclear.

Methods: We conducted a mediation analysis in 2,023 adults from Sleep Heart Health Study Visit 1 with adjudicated dementia outcomes from the Framingham Offspring and Atherosclerosis Risk in Communities cohorts (median follow-up: 21.0 years; 394 events). Exposures included desaturation-removed SpO2 during NREM (non-rapid eye movement) sleep and hypoxic burden (cumulative desaturations ≥2%min/hour); mediators included spindle density, spindle chirp, and spindle-SO coupling phase. Time-to-dementia was modeled using Weibull survival regression with covariate adjustment and demographic stratification; evaluation metrics included C-index and time-dependent area under the curve.

Results: Mean age was 61.5 years; 50.1% were female. One non-White participant was excluded due to potential SpO2 measurement bias. Spindle density significantly mediated both exposures with strong model performance (C-index 0.78 [95% CI: 0.73 - 0.82]; AUC10 0.83 [95% CI: 0.71 - 0.95]). For NREM SpO2, a 90% versus 98% SpO2 was associated with increased spindle density and a 137.0-day delay to dementia diagnosis (95% CI: 10.6-352.1 days; p = 0.024; 26.6% mediated). For hypoxic burden, a 20th percentile (22.35 %min/hour) versus 80th percentile (85.24 %min/hour) burden was correlated with increased spindle density and a 43.4-day delay to dementia diagnosis (95% CI: 1.1-92.9 days; p = 0.046; 69.1% mediated). The SpO2 exposure-mediator correlation was unexpectedly negative, potentially from limited age variability and statistical suppression. Mediation effects remained consistent across covariates and subgroups.

Conclusions: The oxygenation-spindle pathway may represent a physiologic mechanism for time-to-dementia and modifiable marker for established oxygenation interventions.

Study objectives: Cannabis is widely self-administered as a sleep aid, yet objective evidence from large polysomnography cohorts remains scarce. We assessed whether long-term daily cannabis use is associated with alterations in overnight sleep architecture at a Canadian sleep clinic.

Methods: We retrospectively analysed overnight polysomnography studies from 1,449 adult sleep clinic patients. Exposure was chronic cannabis use, defined as ≥ daily consumption for ≥ 1 year (n = 151). Never-users (n = 1,298) served as the reference group. Eleven polysomnography outcomes-total sleep time, sleep onset latency, wake after sleep onset, sleep efficiency, REM latency, and N1, N2, N3, and REM sleep (presence and duration)-were modelled with outcome-appropriate regressions adjusted for 28 demographic, lifestyle, comorbidity, medication, and sleep-related covariates.

Results: Chronic cannabis use was associated with higher wake after sleep onset (β = 21%; 95% CI 6.7% - 37.2%), lower sleep efficiency (β = -3.8%; 95% CI -6.6% - -1.0%), and elevated N1 (β = 2.8 percentage points (pp); 95% CI 0.3pp - 5.6pp). Nominally, total sleeping time was lower among cannabis users (β = -3.3%; 95% CI -6.3% - 0.3%). Effect directions and magnitudes persisted across sensitivity analyses.

Conclusions: Among sleep-clinic patients, long-term daily cannabis use was associated with greater nocturnal wakefulness. Given that most participants had moderate-to-severe sleep apnea, findings should be interpreted with caution. Studies detailing dose, timing, and cannabinoid composition are needed to clarify causality and clinical relevance.

Study objectives: The glymphatic-meningeal lymphatic system plays a crucial role in brain waste clearance. Parasagittal dural space contains meningeal lymphatic vessels. Calcification in the parasagittal dural space is an under-recognized sign. This study aims to explore the potential associations between parasagittal dural space calcification and demographic as well as sleep-related factors.

Methods: In this retrospective study, consecutive patients who visited a sleep clinic between September 2015 and December 2023 were identified. All included individuals underwent a standard polysomnographic examination and a head and neck CT scan. Demographic and anthropometric data, Epworth Sleepiness Scale scores, and polysomnographic measurements were examined as explanatory variables. CT scans were analyzed for the presence of calcifications in the parasagittal dural space. The calcifications were segmented with their volume calculated. Zero-inflated negative binomial regression was used to evaluate the association between calcification volume in the parasagittal dural space and the explanatory variables.

Results: A total of 72 patients (mean age, 41.14 ± 12.72 [standard deviation], 63 men) were included. Of the 72 patients, 17 patients (23.61%) had parasagittal dural space calcification. Multivariate analysis revealed that body mass index (p < 0.001), the duration of stage 3 non-rapid eye movement sleep (p < 0.01) and moderate-to-severe sleep apnea (p = 0.01) were independently associated with calcification volume in the parasagittal dural space.

Conclusion: Higher body mass index, reduced duration of stage 3 non-rapid eye movement sleep and moderate-to-severe sleep apnea were independently associated with a larger volume of calcification in the parasagittal dural space, suggesting a potential link between these factors and impaired meningeal lymphatic function.

Study objectives: While many adults with Long COVID experience sleep problems, the long-term relationship between Long COVID and sleep remains poorly understood. We investigated how Long COVID is prospectively associated with sleep duration, sleep quality, and sleep disturbance using a population-based cohort of Michigan adults with COVID-19 (n=2,406).

Methods: Long COVID was defined at baseline as reporting a recovery time of 90 days or more after the initial infection and sleep outcomes were assessed at follow-up 1 and 2, approximately 1.5 years and 3 years after the initial infection. We estimated linear and multinomial logistic regression models with sleep duration as continuous and categorical variables, respectively. Then, we conducted multinomial logistic regression models for sleep quality and modified Poisson regression for moderate-to-severe sleep disturbance.

Results: Long COVID was prospectively associated with a shorter sleep duration by 0.35 hours (95% CI: -0.53, -0.17) at follow-up 1. Relative to sleeping 6-9 hours, Long COVID was associated with sleeping <6 hours at follow-up 1 (aRRR: 3.27; 95% CI: 2.16, 4.96) and follow-up 2 (aRRR: 1.91; 95% CI: 1.28, 2.85). Additionally, Long COVID had a strong association with poor-to-very poor sleep quality at both follow-up periods relative to very good-to-fair sleep quality at both follow-up periods. Long COVID was also associated with a 1.53 times higher risk of moderate-to-severe sleep disturbance (95% CI: 1.23, 1.91).

Conclusion: Long COVID was prospectively associated with unhealthy sleep outcomes 3 years after onset. There is a need to enhance sleep health among individuals with Long COVID.