ReviewFrontiers in integrative neuroscience2021
Metabolic Disturbances Induced by Sleep Restriction as Potential Triggers for Alzheimer's Disease.
Review in Frontiers in integrative neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Chronic REM Sleep Deprivation Induces Metabolic and Neurotoxic Alterations Associated with Affective and Cognitive Deficit in Male Wistar Rats: Involvement of HPA Axis, Cholinergic, Inflammatory, and Oxidative Stress Pathways.Neurochemical research · 2026Article
- A digital twin framework for predicting and simulating type 2 diabetes onset using retrospective lifestyle data.Frontiers in digital health · 2026Article
- Transcranial near-infrared therapy restores synaptic resilience by reshaping signaling landscapes in sleep-deprived tauopathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- A Sleeping Opportunity Does Not Restore Hippocampal Alterations Induced by 10 Days of Sleep Restriction in Rats.Neurochemical research · 2025Article
- Association between sleep problems and functional disability in community-dwelling older adults.BMC geriatrics · 2024Article
- Sleep deprivation and NLRP3 inflammasome: Is there a causal relationship?Frontiers in neuroscience · 2022Review
- Circadian Synchrony: Sleep, Nutrition, and Physical Activity.Frontiers in network physiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sleep has a major role in learning, memory consolidation, and metabolic function. Although it is known that sleep restriction increases the accumulation of amyloid β peptide (Aβ) and the risk to develop Alzheimer's disease (AD), the mechanism behind these effects remains unknown. In this review, we discuss how chronic sleep restriction induces metabolic and cognitive impairments that could result in the development of AD in late life. Here, we integrate evidence regarding mechanisms whereby metabolic signaling becomes disturbed after short or chronic sleep restriction in the context of cognitive impairment, particularly in the accumulation of Aβ in the brain. We also discuss the role of the blood-brain barrier in sleep restriction with an emphasis on the transport of metabolic signals into the brain and Aβ clearance. This review presents the unexplored possibility that the alteration of peripheral metabolic signals induced by sleep restriction, especially insulin resistance, is responsible for cognitive deficit and, subsequently, implicated in AD development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.