To compare the 24-hour sleep assessment capabilities of two contactless sleep technologies (CSTs) to actigraphy in community-dwelling older adults. We collected 7–14 days of data at home from 35 older adults (age: 65–83), some with medical conditions, using Withings Sleep Analyser (WSA, n = 29), Emfit QS (Emfit, n = 17), a standard actigraphy device (Actiwatch Spectrum [AWS, n = 34]), and a sleep diary (n = 35). We compared nocturnal and daytime sleep measures estimated by the CSTs and actigraphy without sleep diary information (AWS-A) against sleep-diary-assisted actigraphy (AWS|SD). Compared to sleep diary, both CSTs accurately determined the timing of nocturnal sleep (intraclass correlation [ICC]: going to bed, getting out of bed, time in bed >0.75), whereas the accuracy of AWS-A was much lower. Compared to AWS|SD, the CSTs overestimated nocturnal total sleep time (WSA: +92.71 ± 81.16 minutes; Emfit: +101.47 ± 75.95 minutes) as did AWS-A (+46.95 ± 67.26 minutes). The CSTs overestimated sleep efficiency (WSA: +9.19% ± 14.26%; Emfit: +9.41% ± 11.05%), whereas AWS-A estimate (−2.38% ± 10.06%) was accurate. About 65% (n = 23) of participants reported daytime naps either in bed or elsewhere. About 90% in-bed nap periods were accurately determined by WSA while Emfit was less accurate. All three devices estimated 24-hour sleep duration with an error of ≈10% compared to the sleep diary. CSTs accurately capture the timing of in-bed nocturnal sleep periods without the need for sleep diary information. However, improvements are needed in assessing parameters such as total sleep time, sleep efficiency, and naps before these CSTs can be fully utilized in field settings.

Plasma biomarkers of dementia, including phosphorylated tau (p-tau217), offer promise as tools for diagnosis, stratification for clinical trials, monitoring disease progression, and assessing the success of interventions in those living with Alzheimer’s disease. However, currently, it is unknown whether these dementia biomarker levels vary with the time of day, which could have implications for their clinical value. In two protocols, we studied 38 participants (70.8 ± 7.6 years; mean ± SD) in a 27-h laboratory protocol with either two samples taken 12 h apart or 3-hourly blood sampling for 24 h in the presence of a sleep–wake cycle. The study population comprised people living with mild Alzheimer’s disease (PLWA, n = 8), partners/caregivers of PLWA (n = 6) and cognitively intact older adults (n = 24). Single-molecule array technology was used to measure phosphorylated tau (p-tau217) (ALZpath), amyloid-beta 40 (Aβ40), amyloid-beta 42 (Aβ42), glial fibrillary acidic protein, and neurofilament light (NfL) (Neuro 4-Plex E). Analysis with a linear mixed model (SAS, PROC MIXED) revealed a significant effect of time of day for p-tau217, Aβ40, Aβ42, and NfL, and a significant effect of participant group for p-tau217. For p-tau217, the lowest levels were observed in the morning upon waking and the highest values in the afternoon/early evening. The magnitude of the diurnal variation for p-tau217 was similar to the reported increase in p-tau217 over one year in amyloid-β-positive mild cognitively impaired people. Currently, the factors driving this diurnal variation are unknown and could be related to sleep, circadian mechanisms, activity, posture, or meals. Overall, this work implies that the time of day of sample collection may be relevant in the implementation and interpretation of plasma biomarkers in dementia research and care.

Background: Contactless sleep technologies (CSTs) hold promise for longitudinal, unobtrusive sleep monitoring in the community and at scale. They may be particularly useful in older populations wherein sleep disturbance, which may be indicative of the deterioration of physical and mental health, is highly prevalent. However, few CSTs have been evaluated in older people. Objective: This study evaluated the performance of 3 CSTs compared to polysomnography (PSG) and actigraphy in an older population. Methods: Overall, 35 older men and women (age: mean 70.8, SD 4.9 y; women: n=14, 40%), several of whom had comorbidities, including sleep apnea, participated in the study. Sleep was recorded simultaneously using a bedside radar (Somnofy [Vital Things]: n=17), 2 undermattress devices (Withings sleep analyzer [WSA; Withings Inc]: n=35; Emfit-QS [Emfit; Emfit Ltd]: n=17), PSG (n=35), and actigraphy (Actiwatch Spectrum [Philips Respironics]: n=18) during the first night in a 10-hour time-in-bed protocol conducted in a sleep laboratory. The devices were evaluated through performance metrics for summary measures and epoch-by-epoch classification. PSG served as the gold standard. Results: The protocol induced mild sleep disturbance with a mean sleep efficiency (SEFF) of 70.9% (SD 10.4%; range 52.27%-92.60%). All 3 CSTs overestimated the total sleep time (TST; bias: >90 min) and SEFF (bias: >13%) and underestimated wake after sleep onset (bias: >50 min). Sleep onset latency was accurately detected by the bedside radar (bias: 16 min). CSTs did not perform as well as actigraphy in estimating the all-night sleep summary measures. In an epoch-by-epoch concordance analysis, the bedside radar performed better in discriminating sleep versus wake (Matthew correlation coefficient [MCC]: mean 0.63, SD 0.12, 95% CI 0.57-0.69) than the undermattress devices (MCC of WSA: mean 0.41, SD 0.15, 95% CI 0.36-0.46; MCC of Emfit: mean 0.35, SD 0.16, 95% CI 0.26-0.43). The accuracy of identifying rapid eye movement and light sleep was poor across all CSTs, whereas deep sleep (ie, slow wave sleep) was predicted with moderate accuracy (MCC: >0.45) by both Somnofy and WSA. The deep sleep duration estimates of Somnofy correlated (r2=0.60; P<.01) with electroencephalography slow wave activity (0.75-4.5 Hz) derived from PSG, whereas for the undermattress devices, this correlation was not significant (WSA: r2=0.0096, P=.58; Emfit: r2=0.11, P=.21). Conclusions: These CSTs overestimated the TST, and sleep stage prediction was unsatisfactory in this group of older people in whom SEFF was relatively low. Although it was previously shown that CSTs provide useful information on bed occupancy, which may be useful for particular use cases, the performance of these CSTs with respect to the TST and sleep stage estimation requires improvement before they can serve as an alternative to PSG in estimating most sleep variables in older individuals.

Background: Longitudinal monitoring of vital signs provides a method for identifying changes to general health in an individual, particularly in older adults. The nocturnal sleep period provides a convenient opportunity to assess vital signs. Contactless technologies that can be embedded into the bedroom environment are unintrusive and burdenless and have the potential to enable seamless monitoring of vital signs. To realize this potential, these technologies need to be evaluated against gold standard measures and in relevant populations. Objective: We aimed to evaluate the accuracy of heart rate and breathing rate measurements of 3 contactless technologies (2 undermattress trackers, Withings Sleep Analyzer [WSA] and Emfit QS [Emfit]; and a bedside radar, Somnofy) in a sleep laboratory environment and assess their potential to capture vital signs in a real-world setting. Methods: Data were collected from 35 community-dwelling older adults aged between 65 and 83 (mean 70.8, SD 4.9) years (men: n=21, 60%) during a 1-night clinical polysomnography (PSG) test in a sleep laboratory, preceded by 7 to 14 days of data collection at home. Several of the participants (20/35, 57%) had health conditions, including type 2 diabetes, hypertension, obesity, and arthritis, and 49% (17) had moderate to severe sleep apnea, while 29% (n=10) had periodic leg movement disorder. The undermattress trackers provided estimates of both heart rate and breathing rate, while the bedside radar provided only the breathing rate. The accuracy of the heart rate and breathing rate estimated by the devices was compared with PSG electrocardiogram-derived heart rate (beats per minute) and respiratory inductance plethysmography thorax-derived breathing rate (cycles per minute), respectively. We also evaluated breathing disturbance indexes of snoring and the apnea-hypopnea index, available from the WSA. Results: All 3 contactless technologies provided acceptable accuracy in estimating heart rate (mean absolute error <2.12 beats per minute and mean absolute percentage error <5%) and breathing rate (mean absolute error ≤1.6 cycles per minute and mean absolute percentage error <12%) at 1-minute resolution. All 3 contactless technologies were able to capture changes in heart rate and breathing rate across the sleep period. The WSA snoring and breathing disturbance estimates were also accurate compared with PSG estimates (WSA snore: r2=0.76; P<.001; WSA apnea-hypopnea index: r2=0.59; P<.001). Conclusions: Contactless technologies offer an unintrusive alternative to conventional wearable technologies for reliable monitoring of heart rate, breathing rate, and sleep apnea in community-dwelling older adults at scale. They enable the assessment of night-to-night variation in these vital signs, which may allow the identification of acute changes in health, and longitudinal monitoring, which may provide insight into health trajectories. International Registered Report Identifier (IRRID): RR2-10.3390/clockssleep6010010

Sleep and circadian rhythm disturbance are predictors of poor physical and mental health, including dementia. Long-term digital technology-enabled monitoring of sleep and circadian rhythms in the community has great potential for early diagnosis, monitoring of disease progression, and assessing the effectiveness of interventions. Before novel digital technology-based monitoring can be implemented at scale, its performance and acceptability need to be evaluated and compared to gold-standard methodology in relevant populations. Here, we describe our protocol for the evaluation of novel sleep and circadian technology which we have applied in cognitively intact older adults and are currently using in people living with dementia (PLWD). In this protocol, we test a range of technologies simultaneously at home (7–14 days) and subsequently in a clinical research facility in which gold standard methodology for assessing sleep and circadian physiology is implemented. We emphasize the importance of assessing both nocturnal and diurnal sleep (naps), valid markers of circadian physiology, and that evaluation of technology is best achieved in protocols in which sleep is mildly disturbed and in populations that are relevant to the intended use-case. We provide details on the design, implementation, challenges, and advantages of this protocol, along with examples of datasets.

Sleep timing varies between individuals and can be altered in mental and physical health conditions. Sleep and circadian sleep phenotypes, including circadian rhythm sleep-wake disorders, may be driven by endogenous physiological processes, exogeneous environmental light exposure along with social constraints and behavioural factors. Identifying the relative contributions of these driving factors to different phenotypes is essential for the design of personalised interventions.The timing of the human sleep-wake cycle has been modelled as an interaction of a relaxation oscillator (the sleep homeostat), a stable limit cycle oscillator with a near 24-hour period (the circadian process), man-made light exposure and the natural light-dark cycle generated by the Earth’s rotation. However, these models have rarely been used to quantitatively describe sleep at the individual level. Here, we present a new Homeostatic-Circadian-Light model (HCL) which is simpler, more transparent and more computationally efficient than other available models and is designed to run using longitudinal sleep and light exposure data from wearable sensors. We carry out a systematic sensitivity analysis for all model parameters and discuss parameter identifiability.We demonstrate that individual sleep phenotypes in each of 34 older participants (65-83y) can be described by feeding individual participant light exposure patterns into the model and fitting two parameters that capture individual average sleep duration and timing. The fitted parameters describe endogenous drivers of sleep phenotypes.We then quantify exogenous drivers using a novel metric which encodes the circadian phase dependence of the response to light. Combining endogenous and exogeneous drivers better explains individual mean mid-sleep (adjusted R-squared 0.64) than either driver on its own (adjusted R-squared 0.08 and 0.17 respectively).Critically, our model and analysis highlights that different people exhibiting thesamesleep phenotype may havedifferentdriving factors and opens the door to personalised interventions to regularize sleep-wake timing that are readily implementable with current digital health technology.