Alterations in circadian rhythms, such as the daily sleep-wake cycle, are characteristics of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease, and others. Accumulating evidence suggests that sleep disruption is not merely a quality of life issue but also a factor contributing to neurodegeneration and memory impairment. For example, human studies indicate that sleep fragmentation is associated with cognitive decline, preclinical AD neuropathology, and risk of incident AD. Studies in mouse models of AD show that sleep loss interferes with brain clearance of amyloid-beta (Aß) and tau. Furthermore, chronic sleep restriction in mice leads to long-lasting loss of wake-active noradrenergic and orexinergic neurons.
In AD patients, alterations in daily activity rhythms and body temperature rhythms are associated with reduced expression of neuropeptides in the master circadian pacemaker in the hypothalamic suprachiasmatic nucleus (SCN). Circadian rhythms are controlled by transcriptional-translational feedback loops of circadian clock genes, including the essential gene, Bmal1, and others. Age-related attenuation of molecular clock gene rhythms, in the SCN and other brain regions, may increase the risk of AD, because experimental findings in rodents indicate that loss of Bmal1 leads to neurodegeneration. Rodent studies also reveal that enforced wakefulness during normal sleep time induces expression of Per1 and Per2 in the cortex, suggesting a link between sleep disruption and abnormal circadian rhythms.
This Research Topic will explore the role of alterations in sleep-wake rhythms in neurodegeneration as well as the potential therapeutic benefits of enhancing sleep and improving circadian rhythms. Articles reporting new research findings or reviews on topics of related interest are invited for contribution to this Research Topic.
Alterations in circadian rhythms, such as the daily sleep-wake cycle, are characteristics of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease, and others. Accumulating evidence suggests that sleep disruption is not merely a quality of life issue but also a factor contributing to neurodegeneration and memory impairment. For example, human studies indicate that sleep fragmentation is associated with cognitive decline, preclinical AD neuropathology, and risk of incident AD. Studies in mouse models of AD show that sleep loss interferes with brain clearance of amyloid-beta (Aß) and tau. Furthermore, chronic sleep restriction in mice leads to long-lasting loss of wake-active noradrenergic and orexinergic neurons.
In AD patients, alterations in daily activity rhythms and body temperature rhythms are associated with reduced expression of neuropeptides in the master circadian pacemaker in the hypothalamic suprachiasmatic nucleus (SCN). Circadian rhythms are controlled by transcriptional-translational feedback loops of circadian clock genes, including the essential gene, Bmal1, and others. Age-related attenuation of molecular clock gene rhythms, in the SCN and other brain regions, may increase the risk of AD, because experimental findings in rodents indicate that loss of Bmal1 leads to neurodegeneration. Rodent studies also reveal that enforced wakefulness during normal sleep time induces expression of Per1 and Per2 in the cortex, suggesting a link between sleep disruption and abnormal circadian rhythms.
This Research Topic will explore the role of alterations in sleep-wake rhythms in neurodegeneration as well as the potential therapeutic benefits of enhancing sleep and improving circadian rhythms. Articles reporting new research findings or reviews on topics of related interest are invited for contribution to this Research Topic.
