Comparison of single-channel EEG, actigraphy, and sleep diary in cognitively normal and mildly impaired older adults

Abstract

Study Objectives Multiple methods for monitoring sleep-wake activity have identified sleep disturbances as risk factors for Alzheimer disease (AD). In order to identify the level of agreement between different methods, we compared sleep parameters derived from single-channel EEG (scEEG), actigraphy, and sleep diaries in cognitively normal and mildly impaired older adults. Methods 293 participants were monitored at home for up to 6 nights with scEEG, actigraphy, and sleep diaries. Total sleep time (TST), sleep efficiency (SE), sleep onset latency (SOL), and wake after sleep onset (WASO) were calculated using each of these methods. In 109 of the 293 participants, the ratio of cerebrospinal fluid concentrations of phosphorylated tau (p-tau) and amyloid-β-42 (Aβ42) was used as a biomarker for AD pathology. Results Agreement was highest for TST across instruments, especially in cognitively normal older adults. Overall, scEEG and actigraphy appeared to have greater agreement for multiple sleep parameters than for scEEG and diary or actigraphy and diary. Levels of agreement between scEEG and actigraphy overall decreased in mildly impaired participants and those with biomarker evidence of AD pathology, especially for measurements of TST. Conclusions Caution should be exercised when comparing scEEG and actigraphy in individuals with mild cognitive impairment or with AD pathology. Sleep diaries may capture different aspects of sleep compared to scEEG and actigraphy. Additional studies comparing different methods of measuring sleep-wake activity in older adults are necessary to allow for comparison between studies using different methods.

Fragmentation of rest periods, astrocyte activation, and cognitive decline in older adults with and without Alzheimer's disease

“…Ambulatory polysomnography, including EEG, could provide a more definitive differentiation of wake/sleep, provide additional information regarding sleep staging and depth, and identify some causes of sleep fragmentation (e.g., sleep apnea). While several studies have demonstrated the feasibility of ambulatory EEG in adults with mild dementia, 44,45 it remains challenging to obtain ambulatory EEG in adults with more severe dementia, which would be important in a post mortem study such as ours. Third, bulk RNA‐seq cannot distinguish between higher expression of reactive astrocyte genes due to more reactive astrocytes or increased gene expression without change in cell number.…”

Prospective association between sleep duration and cognitive impairment: Findings from the China Health and Retirement Longitudinal Study (CHARLS)

“…Previous cohort studies have investigated the association between sleep duration and cognitive disorders but had inconsistent results, such as the US Nurses’ Health Study by Tworoge et al ( 34 ), the Finnish Twin Cohort by Virta et al ( 35 ), and Screening Across the Lifespan Twin study by Bokenberger et al ( 36 ). Possible reasons included not large sample size ( n < 2,000), short follow-up period (<3 years), or weak in representativeness (e.g., only one sex or twin study).…”

“…Lucey et al investigated the relationship between cognitive performance and sleep duration measured by the single-channel EEG device, and showed that individuals with sleeping less than 4.5 or more than 6.5 h at night had declined cognitive scores (37). Because the sleep time is about one hour shorter measured by EEG than by self-reported, the results corresponded to 5.5-7.5 h per night of self-reported sleep time to have the lowest risk (34,37). Although the biological mechanisms of extreme sleep durations on cognition is still unclear, putative pathways included circadian dysfunction (38), increased accumulation of amyloid-β in the brain (39), and elevate levels of systemic inflammatory markers (e.g., C-reactive protein, interleukin-6) (40)(41)(42).…”

Age differences in the association between sleep and Alzheimer's disease biomarkers in the EPAD cohort

“…The current study is limited by the use of self‐report data, which can be impacted by recall inaccuracies. Subjective sleep measures, particularly of perceived sleep quality, have limited association with more objective sleep measures collected by actigraphy or polysomnography 30 and they do not capture key neurophysiological events integral for optimal sleep and which may provide greater insights into potential disease mechanisms. Additionally, our dataset did not capture obstructive sleep apnea, which is known to be prevalent in older people and linked to AD biomarkers and dementia risk 31 .…”