Evaluating Sleep Deficiency in Persons with Alzheimer's Disease and Related Dementias
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Project Summary Sleep deficiency – defined here as an impairment in sleep duration, architecture, and/or circadian timing – is estimated to be present in up to 70% of persons with Alzheimer's disease and related dementias (ADRD). In this population, sleep deficiency is associated with adverse outcomes, including further cognitive and functional decline, increasing the urgency for accessible tools measuring sleep and circadian timing across the continuum of pre-clinical and clinical phases of ADRD. To advance our understanding of the link between sleep and neurocognitive function in ADRD, feasible, accurate, and comprehensive tools that measure sleep architecture and circadian sleep timing are needed. In addition, there is a paucity of information on the bidirectional relationships between sleep deficiency, biomarkers of neuronal damage and plasticity, and ADRD pathological proteins among persons with ADRD. Elucidating these relationships using measures of sleep architecture and timing would advance mechanistic work and inform interventions to slow progression of ADRD. For my Beeson K76 award, I am evaluating home-based measures of sleep duration, architecture, and circadian timing over multiple days and nights in persons ≥ 60 years. We use a self-applied electroencephalography (EEG)-measuring headband (i.e., an EEG-headband) to assess sleep duration and architecture and enhanced actigraphy measures of circadian sleep timing (e.g., interdaily stability). Now that we have acquired considerable experience in the use of comprehensive and rigorous measures of sleep deficiency in persons without ADRD, we propose to extend this work to persons with ADRD. Working with Yale's Alzheimer's Disease Research Center, we will enroll 45 persons with ADRD to evaluate the performance of the EEG-headband and evaluate cross-sectional relationships between distinct sleep deficiency domains and serum levels of neuronal damage and plasticity (brain derived neurotrophic factor, neurofilament light chain) and ADRD pathological proteins (tau, amyloid-β). The findings from this work will inform the design of a larger, longitudinal study on causal associations between sleep deficiency, neuronal damage/plasticity, and ADRD pathology. Ultimately, this work may elucidate mechanisms, improve prognostication, and establish targets for future sleep-promoting interventions to slow progression of disease and improve quality of life in persons with ADRD.
