Circadian and sleep dysfunction in Alzheimer's disease
Md Sahab Uddin1, Devesh Tewari2, Abdullah Al Mamun1
1Department of Pharmacy, Southeast University, Dhaka, Bangladesh; Pharmakon Neuroscience Research Network, Dhaka, Bangladesh.
Ageing Research Reviews
|March 16, 2020
Summary
Alzheimer's disease (AD) involves cognitive decline and disrupted circadian rhythms. This review explores the mechanistic links between circadian dysfunction, sleep disturbances, and AD pathogenesis, offering therapeutic insights.
Area of Science:
- Neuroscience
- Gerontology
- Pathology
Background:
- Alzheimer's disease (AD) is the most common cause of dementia, characterized by irreversible cognitive decline.
- Dysfunction of circadian rhythms is increasingly recognized as a significant factor in AD progression.
- A complex interplay exists between circadian rhythms, sleep patterns, and the neuropathological hallmarks of AD.
Purpose of the Study:
- To elucidate the mechanistic complexities linking circadian rhythm disruption and sleep deprivation to Alzheimer's disease pathogenesis.
- To review the shared etiopathogenesis between circadian system disturbances and AD.
- To highlight potential therapeutic strategies targeting these pathways.
Main Methods:
- This review synthesizes existing literature on the relationship between circadian rhythms, sleep, and AD.
- Mechanistic insights are drawn from studies investigating amyloid-beta (Aβ) and tau pathology.
- The review examines the impact of aging on sleep and its connection to AD.
Main Results:
- Aging alters sleep quality and timing, exacerbating AD symptoms.
- Increased amyloid-beta (Aβ) production and reduced clearance are linked to sleep disturbances and wakefulness.
- Tau pathology may also significantly contribute to sleep deprivation observed in AD patients.
Conclusions:
- Circadian rhythm dysfunction, sleep deprivation, and AD pathogenesis are interconnected.
- Understanding these mechanisms offers novel therapeutic avenues for AD.
- Targeting sleep and circadian regulation may represent a promising strategy for mitigating AD progression.
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