ArticleSleep2021
Late-in-life neurodegeneration after chronic sleep loss in young adult mice.
Article in Sleep, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Cell-specific effects of acute sleep deprivation on transcriptomic signatures of non-neuronal cells in the mouse hippocampus and prefrontal cortex.bioRxiv : the preprint server for biology · 2026Article
- Self-perceived life course sleep duration trajectories and risk and age at onset of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- A Sleeping Opportunity Does Not Restore Hippocampal Alterations Induced by 10 Days of Sleep Restriction in Rats.Neurochemical research · 2025Article
- Norepinephrine Drives Sleep Fragmentation Activation of Asparagine Endopeptidase, Locus Ceruleus Degeneration, and Hippocampal Amyloid-βThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Experimental laboratory models as tools for understanding modifiable dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Transcranial Irradiation Mitigates Paradoxical Sleep Deprivation Effect in an Age-Dependent Manner: Role of BDNF and GLP-1.Neurochemical research · 2024Article
- Associations of 24-Hour Rest-Activity Rhythm Fragmentation, Cognitive Decline, and Postmortem Locus Coeruleus Hypopigmentation in Alzheimer's Disease.Annals of neurology · 2024Article
- Evaluating Fatty Acid Amide Hydrolase as a Suitable Target for Sleep Promotion in a Transgenic TauP301S Mouse Model of Neurodegeneration.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Association Between Sleep Characteristics and Likelihood of Prodromal Parkinson's Disease: A Cross-Sectional Analysis in the HABIT Study.Nature and science of sleep · 2024Article
- Outdoor nighttime light exposure (light pollution) is associated with Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Review
- Sleep and memory: The impact of sleep deprivation on transcription, translational control, and protein synthesis in the brain.Journal of neurochemistry · 2023Review
- Mutant βProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Early and late chaperone intervention therapy boosts XBP1s and ADAM10, restores proteostasis, and rescues learning in Alzheimer's Disease mice.Aging biology · 2023Article
- Neuropsychological considerations for long-duration deep spaceflight.Frontiers in physiology · 2023Review
- Amide Proton Transfer-Weighted Imaging Detects Hippocampal Proteostasis Disturbance Induced by Sleep Deprivation at 7.0 T MRI.ACS chemical neuroscience · 2022Article
- Potential interactions between cerebellar dysfunction and sleep disturbances in dystonia.Dystonia (Lausanne, Switzerland) · 2022Article
- Neural consequences of chronic sleep disruption.Trends in neurosciences · 2022Review
- Reducing ER stress with chaperone therapy reverses sleep fragmentation and cognitive decline in aged mice.Aging cell · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Chronic short sleep (CSS) is prevalent in modern societies and has been proposed as a risk factor for Alzheimer's disease (AD). In support, short-term sleep loss acutely increases levels of amyloid β (Aβ) and tau in wild type (WT) mice and humans, and sleep disturbances predict cognitive decline in older adults. We have shown that CSS induces injury to and loss of locus coeruleus neurons (LCn), neurons with heightened susceptibility in AD. Yet whether CSS during young adulthood drives lasting Aβ and/or tau changes and/or neural injury later in life in the absence of genetic risk for AD has not been established. Here, we examined the impact of CSS exposure in young adult WT mice on late-in-life Aβ and tau changes and neural responses in two AD-vulnerable neuronal groups, LCn and hippocampal CA1 neurons. Twelve months following CSS exposure, CSS-exposed mice evidenced reductions in CA1 neuron counts and volume, spatial memory deficits, CA1 glial activation, and loss of LCn. Aβ 42 and hyperphosphorylated tau were increased in the CA1; however, amyloid plaques and tau tangles were not observed. Collectively the findings demonstrate that CSS exposure in the young adult mouse imparts late-in-life neurodegeneration and persistent derangements in amyloid and tau homeostasis. These findings occur in the absence of a genetic predisposition to neurodegeneration and demonstrate for the first time that CSS can induce lasting, significant neural injury consistent with some, but not all, features of late-onset AD.
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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.