ArticleJournal of neuroscience research2017
Amyloid-β induces sleep fragmentation that is rescued by fatty acid binding proteins in Drosophila.
Article in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- A Neural-Glial Model of the ApoE-SORT1-FABP7 Axis Tied to Sleep Disruption and Alzheimer's Disease Pathophysiology.Biomolecules · 2025Review
- Cold-raising unmasks sleep disruption in amicroPublication biology · 2025Article
- Enhancing mitochondrial one-carbon metabolism is neuroprotective in Alzheimer's disease models.Cell death & disease · 2024Article
- Neuronal fatty acid-binding protein enhances autophagy and suppresses amyloid-β pathology in a Drosophila model of Alzheimer's disease.PLoS genetics · 2024Article
- Article
- Does glial lipid dysregulation alter sleep in Alzheimer's and Parkinson's disease?Trends in molecular medicine · 2024Review
- Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024Review
- A neuron-glia lipid metabolic cycle couples daily sleep to mitochondrial homeostasis.Nature neuroscience · 2024Article
- Genetic and chemical disruption of amyloid precursor protein processing impairs zebrafish sleep maintenance.iScience · 2024Article
- Circadian disruption and sleep disorders in neurodegeneration.Translational neurodegeneration · 2023Review
- DYRK1a Inhibitor Mediated Rescue ofFrontiers in pharmacology · 2022Article
- A Dichotomous Role for FABP7 in Sleep and Alzheimer's Disease Pathogenesis: A Hypothesis.Frontiers in neuroscience · 2022Article
- Glitazone Treatment Rescues Phenotypic Deficits in a Fly Model of Gaucher/Parkinson's Disease.International journal of molecular sciences · 2021Article
- Sleep disorders in Alzheimer's disease: the predictive roles and potential mechanisms.Neural regeneration research · 2021Review
- Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.PLoS biology · 2021Article
- Parp mutations protect from mitochondrial toxicity in Alzheimer's disease.Cell death & disease · 2021Article
- Aging and the clock: Perspective from flies to humans.The European journal of neuroscience · 2020Review
- Review
- Sleep and circadian rhythm disruption and stress intersect in Alzheimer's disease.Neurobiology of stress · 2019Review
- The neurobiological basis of sleep: Insights from Drosophila.Neuroscience and biobehavioral reviews · 2018Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Disruption of sleep/wake activity in Alzheimer's disease (AD) patients significantly affects their quality of life and that of their caretakers and is a major contributing factor for institutionalization. Levels of amyloid-β (Aβ) have been shown to be regulated by neuronal activity and to correlate with the sleep/wake cycle. Whether consolidated sleep can be disrupted by Aβ alone is not well understood. We hypothesize that Aβ42 can increase wakefulness and disrupt consolidated sleep. Here we report that flies expressing the human Aβ42 transgene in neurons have significantly reduced consolidated sleep compared with control flies. Fatty acid binding proteins (Fabp) are small hydrophobic ligand carriers that have been clinically implicated in AD. Aβ42 flies that carry a transgene of either the Drosophila Fabp or the mammalian brain-type Fabp show a significant increase in nighttime sleep and long consolidated sleep bouts, rescuing the Aβ42-induced sleep disruption. These studies suggest that alterations in Fabp levels and/or activity may be associated with sleep disturbances in AD. Future work to determine the molecular mechanisms that contribute to Fabp-mediated rescue of Aβ42-induced sleep loss will be important for the development of therapeutics in the treatment of AD. © 2016 Wiley Periodicals, Inc.
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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.