ArticlePloS one2011
Fatty-acid binding proteins modulate sleep and enhance long-term memory consolidation in Drosophila.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
- FABP7: A Regulator of Neuro-Immune Metabolic Networks and Therapeutic Vulnerabilities in Glioma.Cancers · 2026Review
- Neuronal fatty acid oxidation fuels memory after intensive learning in Drosophila.Nature metabolism · 2025Article
- A Neural-Glial Model of the ApoE-SORT1-FABP7 Axis Tied to Sleep Disruption and Alzheimer's Disease Pathophysiology.Biomolecules · 2025Review
- The circadian genes are required in DAL neurons forFrontiers in neuroscience · 2025Article
- Neuronal fatty acid-binding protein enhances autophagy and suppresses amyloid-β pathology in a Drosophila model of Alzheimer's disease.PLoS genetics · 2024Article
- A neuron-glia lipid metabolic cycle couples daily sleep to mitochondrial homeostasis.Nature neuroscience · 2024Article
- Article
- FABP7: a glial integrator of sleep, circadian rhythms, plasticity, and metabolic function.Frontiers in systems neuroscience · 2023Article
- Circadian disruption of memory consolidation inFrontiers in systems neuroscience · 2023Article
- Sleep-promoting neurons remodel their response properties to calibrate sleep drive with environmental demands.PLoS biology · 2022Article
- LKB1 is physiologically required for sleep from Drosophila melanogaster to the Mus musculus.Genetics · 2022Article
- Fabp7 Is Required for Normal Sleep Suppression and Anxiety-Associated Phenotype following Single-Prolonged Stress in Mice.Neuroglia (Basel, Switzerland) · 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
- Drosophila fabp is required for light-dependent Rhodopsin-1 clearance and photoreceptor survival.PLoS genetics · 2021Article
- Cannabinoids modulate food preference and consumption in Drosophila melanogaster.Scientific reports · 2021Article
- Article
- Developmental Alcohol Exposure in Drosophila: Effects on Adult Phenotypes and Gene Expression in the Brain.Frontiers in psychiatry · 2021Article
- The Sleep Nullifying Apparatus: A Highly Efficient Method of Sleep Depriving Drosophila.Journal of visualized experiments : JoVE · 2020Article
- The Glial Perspective on Sleep and Circadian Rhythms.Annual review of neuroscience · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Sleep is thought to be important for memory consolidation, since sleep deprivation has been shown to interfere with memory processing. However, the effects of augmenting sleep on memory formation are not well known, and testing the role of sleep in memory enhancement has been limited to pharmacological and behavioral approaches. Here we test the effect of overexpressing the brain-type fatty acid binding protein (Fabp7) on sleep and long-term memory (LTM) formation in Drosophila melanogaster. Transgenic flies carrying the murine Fabp7 or the Drosophila homologue dFabp had reduced baseline sleep but normal LTM, while Fabp induction produced increases in both net sleep and LTM. We also define a post-training consolidation "window" that is sufficient for the observed Fabp-mediated memory enhancement. Since Fabp overexpression increases consolidated daytime sleep bouts, these data support a role for longer naps in improving memory and provide a novel role for lipid-binding proteins in regulating memory consolidation concurrently with changes in behavioral state.
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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.