ArticleBasal ganglia2012
Corticostriatal dysfunction and glutamate transporter 1 (GLT1) in Huntington's disease: interactions between neurons and astrocytes.
Article in Basal ganglia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
- Astrocytes in Neurodegeneration: Spatial States, Crosstalk, and Emerging Therapies.Molecular neurobiology · 2026Review
- Mutant Huntingtin disrupts neurogenic and astroglial programs via the EZH2-Let-7g-LIN28 axis with rescue by epigenetic modulators.Cell death and differentiation · 2026Article
- 3-Nitropropionic Acid-Induced Huntington's Disease in Preclinical Models: Mechanisms, Peripheral Toxicities, Model Gaps, and Future Directions.Molecular neurobiology · 2026Review
- The NMDAR/TRPM4 death complex is a major promoter of disease progression in the 5xFAD mouse model of Alzheimer's disease.Molecular psychiatry · 2026Article
- Photoactivated adenylyl cyclase in cortical astrocytes promotes synaptic potentiation and reveals alterations in Huntington's disease.iScience · 2025Article
- Neural Correlates of Huntington's Disease Based on Electroencephalography (EEG): A Mechanistic Review and Discussion of Excitation and Inhibition (E/I) Imbalance.Journal of clinical medicine · 2025Review
- Interventionally targeting somatic CAG expansions can be a rapid disease-modifying therapeutic avenue: Preclinical evidence.bioRxiv : the preprint server for biology · 2025Article
- Yin Yang 1: Function, Mechanisms, and Glia.Neurochemical research · 2025Review
- Modulation of SNARE-dependent exocytosis in astrocytes improves neuropathology in Huntington's disease.Disease models & mechanisms · 2024Article
- Revisiting the critical roles of reactive astrocytes in neurodegeneration.Molecular psychiatry · 2023Review
- Astrocytic engagement of the corticostriatal synaptic cleft is disrupted in a mouse model of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Astroglial toxicity promotes synaptic degeneration in the thalamocortical circuit in frontotemporal dementia with GRN mutations.The Journal of clinical investigation · 2023Article
- Revealing the contribution of astrocytes to glutamatergic neuronal transmission.Frontiers in cellular neuroscience · 2022Review
- Cannabinoid signaling and risk in Huntington's disease.Frontiers in computational neuroscience · 2022Article
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Striatal network modeling in Huntington's Disease.PLoS computational biology · 2020Article
- Biological Aging and the Cellular Pathogenesis of Huntington's Disease.Journal of Huntington's disease · 2020Review
- Cortical and Striatal Circuits in Huntington's Disease.Frontiers in neuroscience · 2020Review
- Astroglial atrophy in Alzheimer's disease.Pflugers Archiv : European journal of physiology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's Disease (HD) is a fatally inherited neurodegenerative disorder caused by an expanded glutamine repeat in the N-terminal region of the huntingtin (HTT) protein. The result is a progressively worsening triad of cognitive, emotional, and motor alterations that typically begin in adulthood and end in death 10-20 years later. Autopsy of HD patients indicates massive cell loss in the striatum and its main source of input, the cerebral cortex. Further studies of HD patients and transgenic animal models of HD indicate that corticostriatal neuronal processing is altered long before neuronal death takes place. In fact, altered neuronal function appears to be the primary driver of the HD behavioral phenotype, and dysregulation of glutamate, the excitatory amino acid released by corticostriatal afferents, is believed to play a critical role. Although mutant HTT interferes with the operation of multiple proteins related to glutamate transmission, consistent evidence links the expression of mutant HTT with reduced activity of glutamate transporter 1 (rodent GLT1 or human EAAT2), the astrocytic protein responsible for the bulk of glutamate uptake. Here, we review corticostriatal dysfunction in HD and focus on GLT1 and its expression in astrocytes as a possible therapeutic target.
Identifiers
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.