Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 20, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/ijms20040803
Keywords
Alzheimer's disease; sleep disturbance; sleep fragmentation; slow-wave sleep; amyloid beta; tau; proteostasis; default-mode network; cognitive behavioral therapy for insomnia
Funding
- Japan Society for the Promotion of Science, Japan [26860681, 18K15474, 18H02585]
- Japan Foundation for Neuroscience and Mental Health
- Japan Agency for Medical Research and Development and Intramural Research Grants for Neurological and Psychiatric Disorders from NCNP, Japan [JP16ek0109018, JP18ek0109222, 27-9, 30-3]
- Grants-in-Aid for Scientific Research [26860681, 18K15474, 18H02585] Funding Source: KAKEN
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Sleep disturbance is a common symptom in patients with various neurodegenerative diseases, including Alzheimer's disease (AD), and it can manifest in the early stages of the disease. Impaired sleep in patients with AD has been attributed to AD pathology that affects brain regions regulating the sleep-wake or circadian rhythm. However, recent epidemiological and experimental studies have demonstrated an association between impaired sleep and an increased risk of AD. These studies have led to the idea of a bidirectional relationship between AD and impaired sleep; in addition to the conventional concept that impaired sleep is a consequence of AD pathology, various evidence strongly suggests that impaired sleep is a risk factor for the initiation and progression of AD. Despite this recent progress, much remains to be elucidated in order to establish the benefit of therapeutic interventions against impaired sleep to prevent or alleviate the disease course of AD. In this review, we provide an overview of previous studies that have linked AD and sleep. We then highlight the studies that have tested the causal relationship between impaired sleep and AD and will discuss the molecular and cellular mechanisms underlying this link. We also propose future works that will aid the development of a novel disease-modifying therapy and prevention of AD via targeting impaired sleep through non-pharmacological and pharmacological interventions.
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