Association of objective sleep duration with cognition and brain aging biomarkers in older adults

Abstract

The neuropathological mechanisms underlying the association between sleep duration and mild cognitive impairment (MCI) remain poorly understood. This population-based study included 2032 dementia-free people (age ≥ 60 years; 55.1% women) derived from participants in the Multimodal Interventions to Delay Dementia and Disability in Rural China; of these, data were available in 841 participants for Alzheimer’s plasma biomarkers (e.g., amyloid-β[Aβ], total tau, and neurofilament light chain), 1044 for serum microvascular biomarkers (e.g., soluble adhesion molecules), and 834 for brain MRI biomarkers (e.g., whiter matter, grey matter, hippocampus, lacunes, enlarged perivascular spaces [EPVS], and white matter hyperintensity [WMH]). We used electrocardiogram-based cardiopulmonary coupling analysis to measure sleep duration, a neuropsychological test battery to assess cognitive function, and the Petersen’s criteria to define MCI. Data were analysed with multivariable logistic and general linear models. In the total sample (n = 2032), 510 participants were defined with MCI, including 438 with amnestic MCI and 72 with non-amnestic MCI. Long sleep duration (>8 vs. 6-8 hours) was significantly associated with increased likelihoods of MCI and non-amnestic MCI, and lower scores in global cognition, verbal fluency, attention, and executive function (Bonferroni-corrected P < .05). In the subsamples, long sleep duration was associated with higher plasma Aβ40 and total tau, a lower Aβ42/Aβ40 ratio, and smaller grey matter volume (Bonferroni-corrected P < .05). Sleep duration was not significantly associated with serum soluble adhesion molecules, WMH volume, global EPVS, and lacunes (P > .05). Alzheimer’s and neurodegenerative pathologies may represent common pathways linking long sleep duration with MCI and low cognition in older adults.