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 non-rapid-eye-movement (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.
Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA. Electronic address: bamander@berkeley.edu.
Bryce A
BA
Mander
Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA.
Joseph R
JR
Winer
Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720-1650, USA; Molecular Biophysics and Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.
William J
WJ
Jagust
Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720-1650, USA. Electronic address: mpwalker@berkeley.edu.
Matthew P
MP
Walker
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*; D000818:Animals; D006801:Humans; D012890:Sleep / Q000187:drug effects / Q000502:physiology*
Alzheimer's disease; aging; amyloid-β; cognitive decline; sleep