Clifton Lewis

TL;DR: In a sample of cognitively normal elderly, OSA was associated with markers of increased amyloid burden over the 2‐year follow-up, suggesting sleep fragmentation and/or intermittent hypoxia from OSA are likely candidate mechanisms.

TL;DR: In cognitively normal elderly, reduced and fragmented SWS is associated with increases in CSF Aβ42, suggesting that disturbed sleep might drive an increase in soluble brain Aβ levels prior to amyloid deposition.

TL;DR: Orexin-A is associated with increased P-Tau in normal elderly individuals and this might be a consequence of the reduction in the proportion of the deeper, more restorative slow wave sleep and rapid eye movement sleep reported with aging.

TL;DR: This pilot study shows that individuals with CSF biomarkers suggestive of preclinical AD have a higher incidence of EEG abnormalities during sleep than those without, and EEG abnormalities were moderately predictive of elevated p-tau levels.