ArticleCurrent biology : CB2016
Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila.
Article in Current biology : CB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers, 2 of them syntheses that pooled it.
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
55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 citations in OpenAlex.
- Effect of antidiabetic drugs in Alzheimer´s disease: a systematic review of preclinical and clinical studies.Molecular neurodegeneration · 2025Pooled it
- A Systematic Review of Glucose Transport Alterations in Alzheimer's Disease.Frontiers in neuroscience · 2021Pooled it
- Holdfast-Derived Lipid Extract from the Patagonian MacroalgaPharmaceuticals (Basel, Switzerland) · 2026Article
- Metformin alleviates aging-associated periodontitis via NRF2-mediated restoration of the IRE1α dependent unfolded protein response.Bioactive materials · 2026Article
- Human Glucose Transporters in Health and Selected Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- PTPRJ is a negative regulator of insulin signaling in neuronal cells, impacting protein biosynthesis, and neurite outgrowth.Journal of neuroendocrinology · 2024Article
- Glut1 Functions in Insulin-Producing Neurons to Regulate Lipid and Carbohydrate Storage inBiomolecules · 2024Article
- A Retrospective Analysis of Central and Peripheral Metabolic Characteristics in Patients with Cryptococcal Meningitis.Neurology and therapy · 2024Article
- Beneficial effects of metformin treatment on memory impairment.Molecular biology reports · 2024Review
- Glycometabolic Reprogramming of Microglia in Neurodegenerative Diseases: Insights from Neuroinflammation.Aging and disease · 2024Review
- Neuropathogenesis-on-chips for neurodegenerative diseases.Nature communications · 2024Review
- Drug-drug interactions between propofol and ART drugs: Inhibiting neuronal activity by affecting glucose metabolism.CNS neuroscience & therapeutics · 2024Article
- The regulation of triglyceride and glycogen storage by Glucose transporter 1 (microPublication biology · 2024Article
- Amyloid-β specific regulatory T cells attenuate Alzheimer's disease pathobiology in APP/PS1 mice.Molecular neurodegeneration · 2023Article
- Protein retention in the endoplasmic reticulum rescues Aβ toxicity in Drosophila.Neurobiology of aging · 2023Article
- Proteomic alterations in the brain and blood-brain barrier during brain Aβ accumulation in an APP knock-in mouse model of Alzheimer's disease.Fluids and barriers of the CNS · 2023Article
- Apolipoprotein ε in Brain and Retinal Neurodegenerative Diseases.Aging and disease · 2023Review
- A diabetes-like biochemical and behavioural phenotype ofProceedings. Biological sciences · 2023Article
- Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice.Cell reports · 2023Article
- Icariin ameliorates memory deficits through regulating brain insulin signaling and glucose transporters in 3×Tg-AD mice.Neural regeneration research · 2023Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Glucose hypometabolism is a prominent feature of the brains of patients with Alzheimer's disease (AD). Disease progression is associated with a reduction in glucose transporters in both neurons and endothelial cells of the blood-brain barrier. However, whether increasing glucose transport into either of these cell types offers therapeutic potential remains unknown. Using an adult-onset Drosophila model of Aβ (amyloid beta) toxicity, we show that genetic overexpression of a glucose transporter, specifically in neurons, rescues lifespan, behavioral phenotypes, and neuronal morphology. This amelioration of Aβ toxicity is associated with a reduction in the protein levels of the unfolded protein response (UPR) negative master regulator Grp78 and an increase in the UPR. We further demonstrate that genetic downregulation of Grp78 activity also protects against Aβ toxicity, confirming a causal effect of its alteration on AD-related pathology. Metformin, a drug that stimulates glucose uptake in cells, mimicked these effects, with a concomitant reduction in Grp78 levels and rescue of the shortened lifespan and climbing defects of Aβ-expressing flies. Our findings demonstrate a protective effect of increased neuronal uptake of glucose against Aβ toxicity and highlight Grp78 as a novel therapeutic target for the treatment of AD.
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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.