Maria Comas

Light interventions have been investigated for treating sleep disturbances in older adults; however, findings are mixed. This proof‐of‐concept trial investigated the effect of blue‐enriched ambient light on electroencephalographic (EEG) sleep in older adults with self‐reported poor sleep. Twelve participants (65.6 ± 8.7 years) were randomly exposed to two 72‐h in‐laboratory light conditions separated by 2 weeks. During the day, participants were exposed to either blue‐enriched light (intervention: melanopic equivalent daylight illuminance (EDI) = 843.6 lx) or standard light (control: melanopic EDI = 215.8 lx). Three hours before habitual bedtime, illuminance was reduced, with greater blue light attenuation in the intervention (melanopic EDI = 49.5 lx) than control (melanopic EDI = 60.8 lx). On the third night, high‐density EEG sleep, cognitive performance and body temperature were assessed. The primary outcome was wake‐after‐sleep‐onset (WASO). Secondary outcomes included polysomnography‐derived sleep parameters, sleep spindles, cognitive performance and body temperature. High‐density EEG spectral power analyses were exploratory. There was no significant difference in WASO (136.1 ± 52.6 min vs. 117.2 ± 43.9 min; p = 0.338) between intervention and control. Intervention light significantly increased sigma activity (12–16 Hz) during N1 ( p = 0.010) and N2 ( p = 0.017) sleep. The distal‐proximal skin temperature gradient (surrogate of peripheral heat dissipation) before and after lights out increased under intervention compared to control (−1.21°C ± 1.44°C vs. −1.85°C ± 1.39°C, p < 0.001). Daytime enrichment and evening depletion of blue light did not improve objective sleep outcomes in older people with sleep disturbance, but exploratory analyses showed increased sigma activity during sleep. Lighting interventions to improve sleep in older populations require further investigation. Trial Registration: ACTRN12619000138189

Background: Obstructive sleep apnea (OSA) has been implicated in declarative memory impairment. Here, we evaluated immediate recall and overnight declarative memory in patients with suspected OSA before and after standard clinical management in a longitudinal cohort of 265 patients. Methods: A nocturnal polysomnographic study (PSG) was performed at baseline and repeated six months later. The Pictorial-Based Declarative Memory Questionnaire (PDMQ) was administered and consisted of four learning trials followed by free-recall 10 min before PSG and the following morning upon awakening. The primary cognitive endpoint was the change in pictorial declarative memory performance from baseline to 6-month follow-up, expressed as the number of correctly recalled items on the PDMQ. Results: Both immediate and delayed recall performances significantly improved in the no OSA/mild OSA and severe OSA groups, whereas only immediate recall improved in the moderate OSA group. In the severe group, comparisons between patients whose apnea–hypopnea index decreased to 30 revealed significant cognitive improvements in both subgroups, particularly in initial and late trials (Trials 1, 2, 5, 6). In multivariable models, baseline PDMQ performance and indices of SpO₂ desaturation and sleep fragmentation emerged as independent predictors of change in declarative memory. Conclusions: These findings suggest that routine clinical management of patients with OSA was accompanied by modest, albeit statistically significant improvements in declarative memory, and that both intermittent hypoxia and sleep fragmentation play important roles in memory change.

Sleep is a fundamental biological process with broad implications for physical recovery, emotional regulation, and cognitive functioning

Circadian rhythmicity plays a crucial role in regulating sleep timing and continuity, but it may be altered in people with insomnia. This study tested whether dim‐light melatonin onset (DLMO) timing is associated with sleep difficulties in insomnia. In total, 128 people diagnosed with insomnia disorder were recruited. Participants completed daily sleep diaries and wore an actigraph for up to 14 days before the laboratory visit to estimate mean sleep continuity (e.g., sleep latency, sleep duration) and sleep timing (sleep onset time and wake time from diaries, bedtime from diaries and actigraphy). After a sleep study, participants underwent salivary melatonin collection to estimate DLMO on the following night. Regressions and analyses of variances on tertile groups tested associations between DLMO (clock times and phase angle differences between DLMO and sleep timing) and sleep continuity and timing. There were associations between DLMO and sleep timing, r _(s) = 0.27–0.37, but not with sleep continuity. The phase angle between sleep onset time and DLMO was associated with sleep latency, sleep duration, and sleep efficiency, r _(s) = −0.32 to 0.41. Participants with a longer phase angle between DLMO and sleep onset time (> 3 h; i.e., greater delays) had longer sleep latencies ( Mean diff = 43.21 min, SE = 12.99, p = 0.004) and shorter sleep durations ( Mean diff = −65.66 min, SE = 20.75, p = 0.006) than participants with a shorter phase angle (< 2 h). Other phase angles (DLMO and mid‐sleep, wake time) were not consistently associated with sleep continuity. Melatonin onset timing is associated with sleep timing in insomnia disorder. Larger phase angle differences between sleep onset and DLMO are linked to poorer sleep continuity. These findings highlight the importance of considering circadian alignment and its impact on sleep in understanding the pathophysiology of insomnia and in developing targeted treatment interventions.

Background Neurodegenerative synucleinopathies including Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) are strongly associated with sleep disturbances. Furthermore, isolated Rapid Eye Movement Sleep Behaviour Disorder (iRBD) is now established as the strongest risk factor for developing PD or DLB, often preceding the clinical diagnosis by several years. Objectives We aimed to investigate sleep/wake cycles and circadian rhythms in patients with early PD and DLB, along with ‘at risk’ prodromal subjects diagnosed with iRBD. Methods Fifteen healthy controls, 20 iRBD, 16 PD and 17 DLB patients within 5 years of diagnosis, underwent assessment. Sleep/wake cycles were evaluated using questionnaires and actigraphy. Salivary and oral mucosa samples were collected every 3 hours to measure melatonin levels and Bmal1 clock gene expression over 24-hours. Results Both subjective and objective measures of sleep/wake cycles demonstrated that the DLB group exhibited the most significant sleep/wake cycle disruption. In the DLB group, no fundamental sine wave could be fitted to the level of melatonin secretion, indicating a severe disruption in the daily rhythm of this hormone. There was a statistically significant pattern of decreasing median Bmal1 amplitude from HC, to iRBD, to PD and then to DLB (p = 0.037). Conclusions This work highlights a differential gradient of objective disruption in the daily circadian rhythms from iRBD to established PD and DLB and is the first to directly demonstrate disruption of clock gene expression and melatonin in DLB. The findings support sleep/wake disruption as a marker of neuropathological severity and potentially a novel therapeutic target across the synucleinopathy spectrum.

Widefield magnetometry based on nitrogen-vacancy centers enables high spatial resolution imaging of magnetic field distributions without a need for spatial scanning. In this work, we show nitrogen-vacancy center magnetic imaging of Fe₃O₄ nanoparticles within the gastrointestinal tract of Drosophila melanogaster larvae. Vector magnetic field imaging based on optically detected magnetic resonance is carried out on dissected larvae intestine organs containing accumulations of externally loaded magnetic nanoparticles. The distribution of the magnetic nanoparticles within the tissue can be clearly deduced from the magnetic stray field measurements. Spatially resolved magnetic imaging requires the nitrogen-vacancy centers to be very close to the sample making the technique particularly interesting for thin tissue samples. This study is a proof of principle showing the capability of nitrogen-vacancy center magnetometry as a technique to detect magnetic nanoparticle distributions in Drosophila melanogaster larvae that can be extended to other biological systems.

Insomnia is a highly prevalent sleep disorder with strong bidirectional associations with depressive symptoms. The circadian preference for eveningness has been shown to be associated with depressive symptoms in insomnia and other mental health conditions. However, there is a lack of studies in insomnia investigating whether objective measures, such as dim light melatonin onset (DLMO) or polysomnographic (PSG) sleep, are associated with depressive symptoms. Therefore, we investigated the associations between subjective measures (questionnaires assessing anxiety, sleep quality and circadian preference, and sleep diary) and depressive symptoms and whether the addition of objective measures (DLMO, PSG parameters) would strengthen the associations with depressive symptoms. In 115 insomnia disorder patients we found that anxiety was strongly associated with depressive symptoms in a model including circadian preference, dysfunctional beliefs of sleep, and self-reported previous depressive symptoms (R² = 0.496, p < 0.001). The addition of sleep diary measures did not strengthen the model. We also found that the addition of objective measures (DLMO, PSG parameters) did not improve the subjective associations with depressive symptoms. Our data suggest that objective circadian markers are less important in the prediction of depressive symptoms in insomnia compared to subjective measures.

Light therapy is used to treat sleep and circadian rhythm disorders, yet there are limited studies on whether light therapy impacts electroencephalographic (EEG) activity during sleep. Therefore, we aimed to provide an overview of research studies that examined the effects of light therapy on sleep macro- and micro-architecture in populations with sleep and circadian rhythm disorders. We searched for randomized controlled trials that used light therapy and included EEG sleep measures using MEDLINE, PubMed, CINAHL, PsycINFO and Cochrane Central Register of Controlled Trials databases. Five articles met the inclusion criteria of patients with either insomnia or delayed sleep–wake phase disorder (DSWPD). These trials reported sleep macro-architecture outcomes using EEG or polysomnography. Three insomnia trials showed no effect of the timing or intensity of light therapy on total sleep time, wake after sleep onset, sleep efficiency and sleep stage duration compared to controls. Only one insomnia trial reported significantly higher sleep efficiency after evening light therapy (>4000 lx between 21:00–23:00 h) compared with afternoon light therapy (>4000 lx between 15:00–17:00 h). In the only DSWPD trial, six multiple sleep latency tests were conducted across the day (09:00 and 19:00 h) and bright light (2500 lx) significantly lengthened sleep latency in the morning (09:00 and 11:00 h) compared to control light (300 lx). None of the five trials reported any sleep micro-architecture measures. Overall, there was limited research about the effect of light therapy on EEG sleep measures, and studies were confined to patients with insomnia and DSWPD only. More research is needed to better understand whether lighting interventions in clinical populations affect sleep macro- and micro-architecture and objective sleep timing and quality.