ArticleeLife2016
Early dysfunction and progressive degeneration of the subthalamic nucleus in mouse models of Huntington's disease.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Mapping brain volume changes in the zQ175DN mouse model of Huntington's disease: a longitudinal MRI study.Biomarker research · 2026Article
- Development of cognitive, motor, metabolic, and mutant huntingtin aggregation in the zQ175 mouse model of Huntington's disease.Scientific reports · 2025Article
- Movement-related increases in subthalamic activity optimize locomotion.Cell reports · 2024Article
- Reduced thalamic excitation to motor cortical pyramidal tract neurons in parkinsonism.Science advances · 2023Article
- Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023Review
- Subthalamic nucleus shows opposite functional connectivity pattern in Huntington's and Parkinson's disease.Brain communications · 2023Article
- Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Synaptic pathology in Huntington's disease: Beyond the corticostriatal pathway.Neurobiology of disease · 2022Review
- Progression of basal ganglia pathology in heterozygous Q175 knock-in Huntington's disease mice.The Journal of comparative neurology · 2021Article
- Huntington's disease mouse models: unraveling the pathology caused by CAG repeat expansion.Faculty reviews · 2021Review
- Cortical and Striatal Circuits in Huntington's Disease.Frontiers in neuroscience · 2020Review
- Thinking Outside the Box (and Arrow): Current Themes in Striatal Dysfunction in Movement Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Maladaptive Downregulation of Autonomous Subthalamic Nucleus Activity following the Loss of Midbrain Dopamine Neurons.Cell reports · 2019Article
- Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities.Antioxidants & redox signaling · 2019Review
- Mutant Huntingtin Causes a Selective Decrease in the Expression of Synaptic Vesicle Protein 2C.Neuroscience bulletin · 2018Article
- Potassium channel dysfunction in neurons and astrocytes in Huntington's disease.CNS neuroscience & therapeutics · 2018Review
- Alteration of GABAergic neurotransmission in Huntington's disease.CNS neuroscience & therapeutics · 2018Review
- Unravelling and Exploiting Astrocyte Dysfunction in Huntington's Disease.Trends in neurosciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The subthalamic nucleus (STN) is an element of cortico-basal ganglia-thalamo-cortical circuitry critical for action suppression. In Huntington's disease (HD) action suppression is impaired, resembling the effects of STN lesioning or inactivation. To explore this potential linkage, the STN was studied in BAC transgenic and Q175 knock-in mouse models of HD. At <2 and 6 months of age autonomous STN activity was impaired due to activation of K
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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.