11 research outputs found
Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults
Objective: To determine the relationship between sleep quality and CSF markers of Alzheimer disease (AD) pathology in late midlife.
Methods: We investigated the relationship between sleep quality and CSF AD biomarkers in
a cohort enriched for parental history of sporadic AD, the Wisconsin Registry for Alzheimer’s
Prevention. A total of 101 participants (mean age 62.9 6 6.2 years, 65.3% female) completed
sleep assessments and CSF collection and were cognitively normal. Sleep quality was measured
with the Medical Outcomes Study Sleep Scale. CSF was assayed for biomarkers of amyloid
metabolism and plaques (b-amyloid 42 [Ab42]), tau pathology (phosphorylated tau [p-tau]
181), neuronal/axonal degeneration (total tau [t-tau], neurofilament light [NFL]), neuroinflammation/
astroglial activation (monocyte chemoattractant protein–1 [MCP-1], chitinase-3-like protein 1 [YKL40]), and synaptic dysfunction/degeneration (neurogranin). To adjust for individual differences in total
amyloid production, Ab42 was expressed relative to Ab40. To assess cumulative pathology, CSF
biomarkers were expressed in ratio to Ab42. Relationships among sleep scores and CSF biomarkers
were assessed with multiple regression, controlling for age, sex, time between sleep and CSF measurements, and CSF assay batch.
Results: Worse subjective sleep quality, more sleep problems, and daytime somnolence were
associated with greater AD pathology, indicated by lower CSF Ab42/Ab40 and higher t-tau/
Ab42, p-tau/Ab42, MCP-1/Ab42, and YKL-40/Ab42. There were no significant associations
between sleep and NFL or neurogranin.
Conclusions: Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. Effective strategies exist for improving sleep; therefore
sleep health may be a tractable target for early intervention to attenuate AD pathogenesis