ReviewCNS neuroscience & therapeutics2018
Corticostriatal network dysfunction in Huntington's disease: Deficits in neural processing, glutamate transport, and ascorbate release.
Review in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 33 citations in OpenAlex.
- From optical control to translational readiness: an evidence-tiered framework for optogenetics in neuromuscular and neurological disorders.Materials today. Bio · 2026Review
- The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington's disease.Frontiers in aging neuroscience · 2024Review
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Longitudinal multimodal MRI characterization of a knock-in mouse model of Huntington's disease reveals early gray and white matter alterations.Human molecular genetics · 2022Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Emerging Evidence for the Widespread Role of Glutamatergic Dysfunction in Neuropsychiatric Diseases.Nutrients · 2022Review
- Betulinic Acid Hydroxamate is Neuroprotective and Induces Protein Phosphatase 2A-Dependent HIF-1α Stabilization and Post-transcriptional Dephosphorylation of Prolyl Hydrolase 2.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Significant Association Between Huntingtin Gene Mutation and Prevalence of Hopelessness, Depression and Anxiety Symptoms.Acta medica Lituanic · 2021Review
- D1R- and D2R-Medium-Sized Spiny Neurons Diversity: Insights Into Striatal Vulnerability to Huntington's Disease Mutation.Frontiers in cellular neuroscience · 2021Review
- Dysfunction of the corticostriatal pathway in autism spectrum disorders.Journal of neuroscience research · 2020Review
- Cortical and Striatal Circuits in Huntington's Disease.Frontiers in neuroscience · 2020Review
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- The TinyInternational journal of molecular sciences · 2018Review
- Regional differences in dopamine release in the R6/2 mouse caudate putamen.Electroanalysis · 2018Article
- Huntington's disease: From basic science to therapeutics.CNS neuroscience & therapeutics · 2018Article
- Corticostriatal network dysfunction in Huntington's disease: Deficits in neural processing, glutamate transport, and ascorbate release.CNS neuroscience & therapeutics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThis review summarizes evidence for dysfunctional connectivity between cortical and striatal neurons in Huntington's disease (HD), a fatal neurodegenerative condition caused by a single gene mutation. The focus is on data derived from recording of electrophysiological signals in behaving transgenic mouse models. DISCUSSIONS: Firing patterns of individual neurons and the frequency oscillations of local field potentials indicate a disruption in corticostriatal processing driven, in large part, by interactions between cells that contain the mutant gene rather than the mutant gene alone. Dysregulation of glutamate, an excitatory amino acid released by cortical afferents, plays a key role in the breakdown of corticostriatal communication, a process modulated by ascorbate, an antioxidant vitamin found in high concentration in striatum. Up-regulation of glutamate transport by drug administration or viral-vector delivery improves ascorbate homeostasis and neurobehavioral processing in HD mice. Further analysis of electrophysiological data, including the use of sophisticated computational strategies, is required to discern how behavioral demands modulate the flow of corticostriatal information and its disruption by HD.
conclusionsLong before massive cell loss occurs, HD impairs the mechanisms by which cortical and striatal neurons communicate. A key problem identified in transgenic animal models is dysregulation of the dynamic changes in extracellular glutamate and ascorbate. Improved understanding of how these neurochemical systems impact corticostriatal communication is necessary before an effective therapeutic strategy can emerge.
Indexed as
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.