ArticleNeurobiology of sleep and circadian rhythms2017
Enhanced sleep reverses memory deficits and underlying pathology in Drosophila models of Alzheimer's disease.
Article in Neurobiology of sleep and circadian rhythms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 56 citations in OpenAlex.
- β-Amyloid accumulation in the human brain after one night of sleep deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2018Trial
- Progressive behavioral and cognitive decline inbioRxiv : the preprint server for biology · 2026Article
- Article
- Role of d-serine in intestinal ROS accumulation after sleep deprivation.Science advances · 2025Article
- Enhanced memory despite severe sleep loss in Drosophila insomniac mutants.PLoS biology · 2025Article
- Intermittent Vibration Induces Sleep via an Allatostatin A-GABA Signaling Pathway and Provides Broad Benefits in Alzheimer's Disease Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sleep induced by mechanosensory stimulation provides cognitive and health benefits in Drosophila.Sleep · 2024Article
- Sleep induced by mechanosensory stimulation provides cognitive and health benefits inbioRxiv : the preprint server for biology · 2024Article
- Experimental laboratory models as tools for understanding modifiable dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- TDP-43 impairs sleep inScience advances · 2024Article
- Bioelectronic Zeitgebers: targeted neuromodulation to re-establish circadian rhythms.Conference proceedings. IEEE International Conference on Systems, Man, and Cybernetics · 2023Article
- Sleep benefits different stages of memory inFrontiers in physiology · 2023Review
- A brain-wide form of presynaptic active zone plasticity orchestrates resilience to brain aging in Drosophila.PLoS biology · 2022Article
- DYRK1A antagonists rescue degeneration and behavioural deficits of in vivo models based on amyloid-β, Tau and DYRK1A neurotoxicity.Scientific reports · 2022Article
- DYRK1a Inhibitor Mediated Rescue ofFrontiers in pharmacology · 2022Article
- Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.PLoS biology · 2021Article
- Sleep contributes to preference for novel food odours in Drosophila melanogaster.Scientific reports · 2021Article
- Article
- Sleep restores place learning to the adenylyl cyclase mutantJournal of neurogenetics · 2020Article
- Disease-Associated Mutant Tau Prevents Circadian Changes in the Cytoskeleton of Central Pacemaker Neurons.Frontiers in neuroscience · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
To test the hypothesis that sleep can reverse cognitive impairment during Alzheimer's disease, we enhanced sleep in flies either co-expressing human amyloid precursor protein and Beta-secretase (APP:BACE), or in flies expressing human tau. The ubiquitous expression of APP:BACE or human tau disrupted sleep. The sleep deficits could be reversed and sleep could be enhanced when flies were administered the GABA-A agonist 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP). Expressing APP:BACE disrupted both Short-term memory (STM) and Long-term memory (LTM) as assessed using Aversive Phototaxic Suppression (APS) and courtship conditioning. Flies expressing APP:BACE also showed reduced levels of the synaptic protein discs large (DLG). Enhancing sleep in memory-impaired APP:BACE flies fully restored both STM and LTM and restored DLG levels. Sleep also restored STM to flies expressing human tau. Using live-brain imaging of individual clock neurons expressing both tau and the cAMP sensor Epac1-camps, we found that tau disrupted cAMP signaling. Importantly, enhancing sleep in flies expressing human tau restored proper cAMP signaling. Thus, we demonstrate that sleep can be used as a therapeutic to reverse deficits that accrue during the expression of toxic peptides associated with Alzheimer's disease.
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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.