ArticleNature communications2017
Brain microvasculature defects and Glut1 deficiency syndrome averted by early repletion of the glucose transporter-1 protein.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 116 citations in OpenAlex.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- Female-specific alterations in insulin dynamics are associated with glucose tolerance in a Glut1DS mouse model.Disease models & mechanisms · 2026Article
- A therapeutic role for a regulatory GLUT1-associated lncRNA in GLUT1-deficient mice.The Journal of clinical investigation · 2026Article
- Transgenic expression of the human Glucose Transporter1 (GLUT1) gene locus reduces disease burden in Glut1 deficiency syndrome model mice.Neurobiology of disease · 2025Article
- Glut1 Deficiency Syndrome: Novel Pathomechanisms, Current Concepts, and Challenges.Journal of inherited metabolic disease · 2025Review
- Clinical and genetic characteristics of glucose transporter 1 deficiency syndrome in a large cohort of Chinese patients.World journal of pediatrics : WJP · 2025Article
- Diagnosis and treatment recommendations for glucose transporter 1 deficiency syndrome.World journal of pediatrics : WJP · 2025Review
- Enhanced glycolysis causes extracellular acidification and activates acid-sensing ion channel 1a in hypoxic pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Lower GLUT1 and unchanged MCT1 in Alzheimer's disease cerebrovasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- The protective role of endothelial GLUT1 in ischemic stroke.Brain and behavior · 2024Review
- Epileptiform activity in brain organoids derived from patient with Glucose Transporter 1 Deficiency Syndrome.Frontiers in neuroscience · 2024Article
- Effects of Sodium Lactate Infusion in Two Girls with Glucose Transporter 1 Deficiency Syndrome.Neuropediatrics · 2023Article
- Endothelial depletion of Atg7 triggers astrocyte-microvascular disassociation at blood-brain barrier.The Journal of cell biology · 2023Article
- Fibroblast growth factor 18 alleviates stress-induced pathological cardiac hypertrophy in male mice.Nature communications · 2023Article
- Perioperative management of surgical orthodontic treatment in a patient with glucose transporter 1 deficiency: report of a case and review of the literature.Perioperative medicine (London, England) · 2022Article
- Article
- Aberrant Energy Metabolism in Alzheimer's Disease.Journal of translational internal medicine · 2022Article
- Kctd7 deficiency induces myoclonic seizures associated with Purkinje cell death and microvascular defects.Disease models & mechanisms · 2022Article
- Historical and current perspectives on blood endothelial cell heterogeneity in the brain.Cellular and molecular life sciences : CMLS · 2022Review
- In utero exposure to maternal anti-aquaporin-4 antibodies alters brain vasculature and neural dynamics in male mouse offspring.Science translational medicine · 2022Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
Abstract
Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood-brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS.
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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.