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Circadian and sleep dysfunction in Alzheimer's disease

dc.contributor.authorUddin M.S.
dc.contributor.authorTewari D.
dc.contributor.authorMamun A.A.
dc.contributor.authorKabir M.T.
dc.contributor.authorNiaz K.
dc.contributor.authorWahed M.I.I.
dc.contributor.authorBarreto G.E.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:29:30Z
dc.date.available2020-09-02T22:29:30Z
dc.date.issued2020
dc.identifier10.1016/j.arr.2020.101046
dc.identifier.citation60, , -
dc.identifier.issn15681637
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6468
dc.descriptionAlzheimer's disease (AD) is a devastating and irreversible cognitive impairment and the most common type of dementia. Along with progressive cognitive impairment, dysfunction of the circadian rhythms also plays a pivotal role in the progression of AD. A mutual relationship among circadian rhythms, sleep, and AD has been well-recommended. The etiopathogenesis of the disturbances of the circadian system and AD share some general features that also unlock the outlook of observing them as a mutually dependent pathway. Indeed, the burden of amyloid β (Aβ), neurofibrillary tangles (NFTs), neuroinflammation, oxidative stress, and dysfunction of circadian rhythms may lead to AD. Aging can alter both sleep timings and quality that can be strongly disrupted in AD. Increased production of Aβ and reduced Aβ clearance are caused by a close interplay of Aβ, sleep disturbance and raised wakefulness. Besides Aβ, the impact of tau pathology is possibly noteworthy to the sleep deprivation found in AD. Hence, this review is focused on the primary mechanistic complexities linked to disruption of circadian rhythms, sleep deprivation, and AD. Furthermore, this review also highlights the potential therapeutic strategies to abate AD pathogenesis. © 2020 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.subjectAlzheimer's disease
dc.subjectAmyloid β
dc.subjectCircadian rhythms
dc.subjectNeurofibrillary tangles
dc.subjectSleep
dc.subjectalmorexant
dc.subjectamyloid
dc.subjectamyloid beta protein
dc.subjectcholinergic receptor
dc.subjecthypnotic agent
dc.subjectmelanopsin
dc.subjectmelatonin
dc.subjectorexin
dc.subjectPittsburgh compound B
dc.subjectramelteon
dc.subjecttasimelteon
dc.subjecttau protein
dc.subjecttranscription factor CLOCK
dc.subjecttrazodone
dc.subjectAlzheimer disease
dc.subjectamyloid plaque
dc.subjectbasal forebrain
dc.subjectbiological rhythm
dc.subjectblood pressure
dc.subjectbody temperature
dc.subjectbright light therapy
dc.subjectcell loss
dc.subjectchronobiology
dc.subjectcircadian rhythm
dc.subjectcognition
dc.subjectcross-sectional study
dc.subjectdaytime somnolence
dc.subjectexercise
dc.subjectfeeding behavior
dc.subjecthistopathology
dc.subjecthuman
dc.subjectinsomnia
dc.subjectmolecular clock
dc.subjectnerve degeneration
dc.subjectnervous system inflammation
dc.subjectneurofibrillary tangle
dc.subjectneuropathology
dc.subjectneuroprotection
dc.subjectnoise
dc.subjectnonhuman
dc.subjectoxidation reduction state
dc.subjectoxidative stress
dc.subjectpathogenesis
dc.subjectphototherapy
dc.subjectphysical activity
dc.subjectpositron emission tomography
dc.subjectprescription
dc.subjectprotein depletion
dc.subjectprotein phosphorylation
dc.subjectretina ganglion cell
dc.subjectReview
dc.subjectsleep
dc.subjectsleep deprivation
dc.subjectsleep disorder
dc.subjectsleep hygiene
dc.subjectsleep pattern
dc.subjectsleep waking cycle
dc.subjectwakefulness
dc.titleCircadian and sleep dysfunction in Alzheimer's disease
dc.typeReview


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