ReviewJournal of Huntington's disease2016
Dysregulation of Corticostriatal Connectivity in Huntington's Disease: A Role for Dopamine Modulation.
Review in Journal of Huntington's disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 47 citations in OpenAlex.
- From optical control to translational readiness: an evidence-tiered framework for optogenetics in neuromuscular and neurological disorders.Materials today. Bio · 2026Review
- SOM3355: a unique pharmacological profile combining VMAT1 inhibition, VMAT2-mediated dopamine modulation, and βFrontiers in pharmacology · 2026Article
- Advances in Brain Stimulation, Nanomedicine and the Use of Magnetoelectric Nanoparticles: Dopaminergic Alterations and Their Role in Neurodegeneration and Drug Addiction.Molecules (Basel, Switzerland) · 2024Review
- Risk Factors and Interventions for Suicide in Huntington's Disease-A Systematic Review.Journal of clinical medicine · 2024Review
- Mild cognitive impairment in Huntington's disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Regulation of one-carbon metabolism may open new avenues to slow down the initiation and progression of Huntington's disease.Neural regeneration research · 2023Article
- Ex vivo 100 μm isotropic diffusion MRI-based tractography of connectivity changes in the end-stage R6/2 mouse model of Huntington's disease.Neuroprotection (Chichester, England) · 2023Article
- Mitochondrial Dysfunction in Repeat Expansion Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- hESC-derived striatal progenitors grafted into a Huntington's disease rat model support long-term functional motor recovery by differentiating, self-organizing and connecting into the lesioned striatum.Stem cell research & therapy · 2023Article
- Modulating and monitoring the functionality of corticostriatal circuits using an electrostimulable microfluidic device.Molecular brain · 2023Article
- Huntington disease exacerbates action impulses.Frontiers in psychology · 2023Article
- A plant-based mutant huntingtin model-driven discovery of impaired expression of GTPCH and DHFR.Cellular and molecular life sciences : CMLS · 2022Article
- Age-Dependent Degradation of Locomotion Encoding in Huntington's Disease R6/2 Model Mice.Journal of Huntington's disease · 2021Article
- No symphony without bassoon and piccolo: changes in synaptic active zone proteins in Huntington's disease.Acta neuropathologica communications · 2020Article
- Cortical and Striatal Circuits in Huntington's Disease.Frontiers in neuroscience · 2020Review
- Insulin and Exendin-4 Reduced Mutated Huntingtin Accumulation in Neuronal Cells.Frontiers in pharmacology · 2020Article
- Lack of mutant huntingtin in cortical efferents improves behavioral inflexibility and corticostriatal dynamics in Huntington's disease mice.Journal of neurophysiology · 2019Article
- Mutant huntingtin disrupts mitochondrial proteostasis by interacting with TIM23.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Roles of the MMovement disorders : official journal of the Movement Disorder Society · 2019Review
- NIR Biosensing of Neurotransmitters in Stem Cell-Derived Neural Interface Using Advanced Core-Shell Upconversion Nanoparticles.Advanced materials (Deerfield Beach, Fla.) · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant communication between striatum, the main information processing unit of the basal ganglia, and cerebral cortex plays a critical role in the emergence of Huntington's disease (HD), a fatal monogenetic condition that typically strikes in the prime of life. Although both striatum and cortex undergo substantial cell loss over the course of HD, corticostriatal circuits become dysfunctional long before neurons die. Understanding the dysfunction is key to developing effective strategies for treating a progressively worsening triad of motor, cognitive, and psychiatric symptoms. Cortical output neurons drive striatal activity through the release of glutamate, an excitatory amino acid. Striatal outputs, in turn, release γ-amino butyric acid (GABA) and exert inhibitory control over downstream basal ganglia targets. Ample evidence from transgenic rodent models points to dysregulation of corticostriatal glutamate transmission along with corresponding changes in striatal GABA release as underlying factors in the HD behavioral phenotype. Another contributor is dysregulation of dopamine (DA), a modulator of both glutamate and GABA transmission. In fact, pharmacological manipulation of DA is the only currently available treatment for HD symptoms. Here, we review data from animal models and human patients to evaluate the role of DA in HD, including DA interactions with glutamate and GABA within the context of dysfunctional corticostriatal circuitry.
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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.