Circadian and sleep dysfunction in Alzheimer's disease

Md Sahab Uddin*, Devesh Tewari, Abdullah Al Mamun, Md Tanvir Kabir, Kamal Niaz, Mir Imam Ibne Wahed, George E. Barreto, Ghulam Md Ashraf

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

116 Citations (Scopus)

Abstract

Alzheimer'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.

Original languageEnglish
Article number101046
JournalAgeing Research Reviews
Volume60
DOIs
Publication statusPublished - Jul 2020
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid β
  • Circadian rhythms
  • Neurofibrillary tangles
  • Sleep

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