ArticleNature neuroscience2011
The neural substrates of rapid-onset Dystonia-Parkinsonism.
Article in Nature neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 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
149 citing papers in PubMed, 258 citations in OpenAlex.
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- Chronic Administration of Marinobufagenin in Mice Causes Hyperlocomotion and Decrease in Anxiety by Altering Monoamine Turnover Unaccompanied by Motor Deficits or Oxidative Stress.International journal of molecular sciences · 2026Article
- Human and mouse cerebellar inhibitory circuits in dystonic crisis and their modulation with therapeutic stimulation.bioRxiv : the preprint server for biology · 2026Article
- Cerebellar motor and non-motor contributions to dystonia pathophysiology and treatment.Dystonia (Lausanne, Switzerland) · 2026Article
- The Second Hit Hypothesis in Animal and Human Dystonia: The Role of Peripheral Nerve Trauma and Spinal Cord Injury.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- Validation of a torsinA cerebellar knockdown model of DYT1 dystonia.Dystonia (Lausanne, Switzerland) · 2026Article
- Mapping the Neuroanatomy of Dystonia Using Causal Brain Lesions.medRxiv : the preprint server for health sciences · 2025Article
- Cerebellar dysfunction in a mouse model of childhood-onset manganese-induced dystonia parkinsonism.Neurobiology of disease · 2025Article
- Exploring the relationship between dystonia and STN-DBS in Parkinson's disease: insights from a single-centre cohort.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Neurobiology of Dystonia: Review of Genetics, Animal Models, and Neuroimaging.Brain sciences · 2025Review
- Aberrant outputs of glutamatergic neurons in deep cerebellar nuclei mediate dystonic movements.Science advances · 2025Article
- ATP1A3 dysfunction causes motor hyperexcitability and afterhyperpolarization loss in a dystonia model.Brain : a journal of neurology · 2025Article
- Thalamic deep brain stimulation improves movement in a cerebellar model of lesion-based status dystonicus.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei.Dystonia (Lausanne, Switzerland) · 2025Article
- Mutation in Prkra results in cerebellar abnormality and reduced eIF2α phosphorylation in a model of DYT-PRKRA.Disease models & mechanisms · 2024Article
- Review
- Article
- Sensory-motor circuit is a therapeutic target forScience advances · 2024Article
- Slow G-Quadruplex Conformation Rearrangement and Accessibility Change Induced by Potassium in Human Telomeric Single-Stranded DNA.The journal of physical chemistry. B · 2024Article
- A frameshift mutation in the murinebioRxiv : the preprint server for biology · 2024Article
89 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although dystonias are a common group of movement disorders, the mechanisms by which brain dysfunction results in dystonia are not understood. Rapid-onset Dystonia-Parkinsonism (RDP) is a hereditary dystonia caused by mutations in the ATP1A3 gene. Affected individuals can be free of symptoms for years, but rapidly develop persistent dystonia and Parkinsonism-like symptoms after a stressful experience. Using a mouse model, we found that an adverse interaction between the cerebellum and basal ganglia can account for the symptoms of these individuals. The primary instigator of dystonia was the cerebellum, whose aberrant activity altered basal ganglia function, which in turn caused dystonia. This adverse interaction between the cerebellum and basal ganglia was mediated through a di-synaptic thalamic pathway that, when severed, alleviated dystonia. Our results provide a unifying hypothesis for the involvement of cerebellum and basal ganglia in the generation of dystonia and suggest therapeutic strategies for the treatment of RDP.
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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.