Sleep · 2024
Associations of sleep duration and daytime sleepiness with plasma amyloid beta and cognitive performance in cognitively unimpaired, middle-aged and older African Americans.
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Cook Jesse D, Malik Ammara, Plante David T, Norton Derek, Langhough Koscik Rebecca, Du Lianlian, Bendlin Barbara B, Kirmess Kris M, Holubasch Mary S, Meyer Matthew R, Venkatesh Venky, West Tim, Verghese Philip B, Yarasheski Kevin E, Thomas Kevin V, Carlsson Cynthia M, Asthana Sanjay, Johnson Sterling C, Gleason Carey E, Zuelsdorff Megan
Аннотация
STUDY OBJECTIVES: Given the established racial disparities in both sleep health and dementia risk for African American populations, we assess cross-sectional and longitudinal associations of self-report sleep duration (SRSD) and daytime sleepiness with plasma amyloid beta (Aβ) and cognition in an African American (AA) cohort.
METHODS: In a cognitively unimpaired sample drawn from the African Americans Fighting Alzheimer's in Midlife (AA-FAiM) study, data on SRSD, Epworth Sleepiness Scale, demographics, and cognitive performance were analyzed. Aβ40, Aβ42, and the Aβ42/40 ratio were quantified from plasma samples. Cross-sectional analyses explored associations between baseline predictors and outcome measures. Linear mixed-effect regression models estimated associations of SRSD and daytime sleepiness with plasma Aβ and cognitive performance levels and change over time.
RESULTS: One hundred and forty-seven participants comprised the cross-sectional sample. Baseline age was 63.2 ± 8.51 years. 69.6% self-identified as female. SRSD was 6.4 ± 1.1 hours and 22.4% reported excessive daytime sleepiness. The longitudinal dataset included 57 participants. In fully adjusted models, neither SRSD nor daytime sleepiness is associated with cross-sectional or longitudinal Aβ. Associations with level and trajectory of cognitive test performance varied by measure of sleep health.
CONCLUSIONS: SRSD was below National Sleep Foundation recommendations and daytime sleepiness was prevalent in this cohort. In the absence of observed associations with plasma Aβ, poorer self-reported sleep health broadly predicted poorer cognitive function but not accelerated decline. Future research is necessary to understand and address modifiable sleep mechanisms as they relate to cognitive aging in AA at disproportionate risk for dementia.
CLINICAL TRIAL INFORMATION: Not applicable.
METHODS: In a cognitively unimpaired sample drawn from the African Americans Fighting Alzheimer's in Midlife (AA-FAiM) study, data on SRSD, Epworth Sleepiness Scale, demographics, and cognitive performance were analyzed. Aβ40, Aβ42, and the Aβ42/40 ratio were quantified from plasma samples. Cross-sectional analyses explored associations between baseline predictors and outcome measures. Linear mixed-effect regression models estimated associations of SRSD and daytime sleepiness with plasma Aβ and cognitive performance levels and change over time.
RESULTS: One hundred and forty-seven participants comprised the cross-sectional sample. Baseline age was 63.2 ± 8.51 years. 69.6% self-identified as female. SRSD was 6.4 ± 1.1 hours and 22.4% reported excessive daytime sleepiness. The longitudinal dataset included 57 participants. In fully adjusted models, neither SRSD nor daytime sleepiness is associated with cross-sectional or longitudinal Aβ. Associations with level and trajectory of cognitive test performance varied by measure of sleep health.
CONCLUSIONS: SRSD was below National Sleep Foundation recommendations and daytime sleepiness was prevalent in this cohort. In the absence of observed associations with plasma Aβ, poorer self-reported sleep health broadly predicted poorer cognitive function but not accelerated decline. Future research is necessary to understand and address modifiable sleep mechanisms as they relate to cognitive aging in AA at disproportionate risk for dementia.
CLINICAL TRIAL INFORMATION: Not applicable.