ArticlePLoS genetics2018
AMPK signaling linked to the schizophrenia-associated 1q21.1 deletion is required for neuronal and sleep maintenance.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- The Association of Environmental Variables with Intelligence and Well-Being in Copy Number Variation (CNV) Carriers.Research square · 2026Article
- Article
- Dissecting metabolic regulation of behaviors and physiology during aging in Drosophila.Biogerontology · 2025Article
- A genome-wide pleiotropy study between atopic dermatitis and neuropsychiatric disorders.Human genomics · 2025Article
- Repurposing Caffeine, Metformin, and Furosemide to Target Schizophrenia-Related Impairments in a Triple-Hit Rat Model.International journal of molecular sciences · 2025Article
- Peering into the mind: unraveling schizophrenia's secrets using models.Molecular psychiatry · 2025Review
- Calcium/calmodulin-dependent protein kinase II α and β differentially regulate mammalian sleep.Communications biology · 2025Article
- A review on the relationship between the distal 1q21.1 microdeletion and schizophrenia.Frontiers in genetics · 2025Review
- A genetic-epigenetic interplay at 1q21.1 locus underlies CHD1L-mediated vulnerability to primary progressive multiple sclerosis.Nature communications · 2024Article
- Potential Schizophrenia Disease-Related Genes Prediction Using Metagraph Representations Based on a Protein-Protein Interaction Keyword Network: Framework Development and Validation.JMIR formative research · 2023Article
- A New Concept of Associations between Gut Microbiota, Immunity and Central Nervous System for the Innovative Treatment of Neurodegenerative Disorders.Metabolites · 2022Article
- A gut-derived hormone suppresses sugar appetite and regulates food choice in Drosophila.Nature metabolism · 2022Article
- LKB1 is physiologically required for sleep from Drosophila melanogaster to the Mus musculus.Genetics · 2022Article
- Dissecting the complexity of CNV pathogenicity: insights from Drosophila and zebrafish models.Current opinion in genetics & development · 2021Review
- Dissecting Molecular Genetic Mechanisms of 1q21.1 CNV in Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- Identify specific gene pairs for subarachnoid hemorrhage based on wavelet analysis and genetic algorithm.PloS one · 2021Article
- AMPK and the Need to Breathe and Feed: What's the Matter with Oxygen?International journal of molecular sciences · 2020Review
- Analysis of genes within the schizophrenia-linked 22q11.2 deletion identifies interaction of night owl/LZTR1 and NF1 in GABAergic sleep control.PLoS genetics · 2020Article
- Time-Varying Gene Network Analysis of Human Prefrontal Cortex Development.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human 1q21.1 deletion of ten genes is associated with increased risk of schizophrenia. This deletion involves the β-subunit of the AMP-activated protein kinase (AMPK) complex, a key energy sensor in the cell. Although neurons have a high demand for energy and low capacity to store nutrients, the role of AMPK in neuronal physiology is poorly defined. Here we show that AMPK is important in the nervous system for maintaining neuronal integrity and for stress survival and longevity in Drosophila. To understand the impact of this signaling system on behavior and its potential contribution to the 1q21.1 deletion syndrome, we focused on sleep, an important role of which is proposed to be the reestablishment of neuronal energy levels that are diminished during energy-demanding wakefulness. Sleep disturbances are one of the most common problems affecting individuals with psychiatric disorders. We show that AMPK is required for maintenance of proper sleep architecture and for sleep recovery following sleep deprivation. Neuronal AMPKβ loss specifically leads to sleep fragmentation and causes dysregulation of genes believed to play a role in sleep homeostasis. Our data also suggest that AMPKβ loss may contribute to the increased risk of developing mental disorders and sleep disturbances associated with the human 1q21.1 deletion.
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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.