ArticleeLife2020
Sleep is bi-directionally modified by amyloid beta oligomers.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Comparison of safety of lecanemab and donanemab: a real-world disproportionality analysis using the FDA adverse event reporting system.Frontiers in pharmacology · 2026Article
- Partial normalization of hippocampal oscillatory activity during sleep in TgF344-AD rats coincides with increased cholinergic synapses at early-plaque stage of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Cold-raising unmasks sleep disruption in amicroPublication biology · 2025Article
- Genetic and chemical disruption of amyloid precursor protein processing impairs zebrafish sleep maintenance.iScience · 2024Article
- Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry.Journal of Alzheimer's disease : JAD · 2024Review
- Zebrafish as a Model Organism for Studying Pathologic Mechanisms of Neurodegenerative Diseases and other Neural Disorders.Cellular and molecular neurobiology · 2023Review
- Multimodal investigation of melanopsin retinal ganglion cells in Alzheimer's disease.Annals of clinical and translational neurology · 2023Article
- Proteostasis failure exacerbates neuronal circuit dysfunction and sleep impairments in Alzheimer's disease.Molecular neurodegeneration · 2023Review
- Review
- How to Prevent and/or Revert Alzheimer's Disease Continuum During Preclinical Phases.Journal of Alzheimer's disease reports · 2023Review
- Progressive sleep disturbance in various transgenic mouse models of Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- The Link between Obstructive Sleep Apnea and Neurocognitive Impairment: An Official American Thoracic Society Workshop Report.Annals of the American Thoracic Society · 2022Article
- Association of rs3027178 polymorphism in the circadian clock gene PER1 with susceptibility to Alzheimer's disease and longevity in an Italian population.GeroScience · 2022Article
- Zebrafish as a Tool in the Study of Sleep and Memory-related Disorders.Current neuropharmacology · 2022Review
- Large-scale Analysis of Sleep in Zebrafish.Bio-protocol · 2022Article
- Validation of Candidate Sleep Disorder Risk Genes Using Zebrafish.Frontiers in molecular neuroscience · 2022Review
- Article
- Differential Clearance of Aβ Species from the Brain by Brain Lymphatic Endothelial Cells in Zebrafish.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Disrupted sleep is a major feature of Alzheimer's disease (AD), often arising years before symptoms of cognitive decline. Prolonged wakefulness exacerbates the production of amyloid-beta (Aβ) species, a major driver of AD progression, suggesting that sleep loss further accelerates AD through a vicious cycle. However, the mechanisms by which Aβ affects sleep are unknown. We demonstrate in zebrafish that Aβ acutely and reversibly enhances or suppresses sleep as a function of oligomer length. Genetic disruptions revealed that short Aβ oligomers induce acute wakefulness through Adrenergic receptor b2 (Adrb2) and Progesterone membrane receptor component 1 (Pgrmc1), while longer Aβ forms induce sleep through a pharmacologically tractable Prion Protein (PrP) signaling cascade. Our data indicate that Aβ can trigger a bi-directional sleep/wake switch. Alterations to the brain's Aβ oligomeric milieu, such as during the progression of AD, may therefore disrupt sleep via changes in acute signaling events.
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What OpenQuestion holds
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.