Abstract
Alzheimer's disease (AD) is a neurodegenerative disease that accounts for most cases of dementia. Besides progressive cognitive decline, circadian dysfunction is a prominent feature of AD. Circadian disruption is traditionally regarded as a downstream symptom of AD, but recent evidence suggests that circadian dysregulation may act to exacerbate AD pathology. A reciprocal link among sleep, circadian rhythms, and amyloid deposition has long been suspected, and data from both human and animal studies support this hypothesis. The sleep-wake cycle regulates amyloid-beta (Aβ) levels in both mice and humans. Sleep deprivation increases Aβ levels in mice, and sleep apnea and insomnia may be related to AD in humans. Furthermore, melatonin, the principal hormonal output of the circadian system, is dysregulated in AD, and this may be important because melatonin is protective in cells exposed to toxic Aβ. Initial evidence supports a reciprocal link among sleep, circadian rhythmicity, and AD. More investigation is necessary to replicate these studies and determine the extent to which the circadian system contributes to the pathogenesis of AD.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease that accounts for most cases of dementia
This study provided direct evidence that sleep and the circadian system may have a role in the pathogenesis of AD
As sleep is associated with a net decrease in synaptic strength whereas wakefulness is associated with a net increase [14], the circadian sleep-wake cycle may act to modulate Aβ levels via changes in neuronal activity
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease that accounts for most cases of dementia. In AD, excessive Aβ accumulates and aggregates into plaques, which contribute to progressive cognitive deficits. Circadian dysfunction is another prominent feature of AD, and recent evidence suggests. Circadian dysfunction is implicated in the pathology of several other disease states as well. Major depression may be associated with sleep disruption, diurnal mood swings, and elevated nocturnal body temperature; manipulation of sleep and the circadian cycle is an effective, though short-lasting, treatment. Manipulation of the circadian light-dark cycle causes direct changes to brain structure and function [3]. AD is associated with circadian dysfunction, but the extent to which these changes constitute symptoms, disease pathogenesis, or both remains unspecified. Is article will present evidence in support of a reciprocal relationship between the circadian system and AD pathology
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