Is poor sleep linked to Alzheimer's biomarkers before symptoms appear?

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Sleep abnormalities are common in Alzheimer's disease, and sleep quality is already impaired at the preclinical stage. Epidemiological and experimental evidence suggests that sleep abnormalities may contribute to Alzheimer's risk. Earlier studies, however, were limited by a lack of Alzheimer's biomarkers, small samples or cross-sectional designs. Understanding whether, when and how poor sleep contributes to disease progression could help target therapies to the right phase.

Using what they described as the largest cohort to date, the European Prevention of Alzheimer's Dementia Longitudinal Cohort Study, researchers tested whether poor sleep was associated with core Alzheimer's biomarkers in cerebrospinal fluid (CSF) at one point in time and predicted future increases in Alzheimer's pathology among people without identifiable Alzheimer's symptoms at baseline. The study included 1,168 adults over age 50 with data on core CSF biomarkers—total tau, phosphorylated tau and amyloid-beta—cognitive performance and sleep quality measured with the Pittsburgh Sleep Quality Index questionnaire. The researchers used multivariate linear regressions to examine associations between the biomarkers and the index's total sleep-quality score, a binary score defining poor sleep as greater than 5, sleep latency, duration, efficiency and disturbance. In a subsample of 332 participants who provided CSF at baseline and after an average of 1.5 years, they assessed how baseline sleep quality related to changes in biomarkers over time.

In cross-sectional analyses, poor sleep quality (a total score greater than 5) was significantly associated with higher CSF total tau; sleep duration under 7 hours was associated with higher CSF phosphorylated tau and total tau; and greater sleep disturbance (scores of 1–9 versus 0 and greater than 9 versus 0) was associated with lower CSF amyloid-beta. Longitudinally, greater sleep disturbance (1–9 versus 0 and greater than 9 versus 0) was associated with a decrease in CSF Aβ42 over time. The authors concluded that self-reported poor sleep quality was associated with greater Alzheimer's-related pathology in cognitively unimpaired individuals, and that the longitudinal results further supported the hypothesis that disrupted sleep may be a risk factor for Alzheimer's disease. They called for future studies to test whether preventive practices that improve sleep before symptoms appear can reduce Alzheimer's pathology.