Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer's Disease?

Sleep disruption appears to be a core component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-β (Aβ), potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals, evaluating: (i) associations and plausible mechanisms linking NREM sleep disruption, Aβ, and AD, (ii) a role for NREM sleep disruption as a novel factor linking cortical Aβ to impaired hippocampus-dependent memory consolidation, (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD, and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits