ReviewNeuroscience letters2019
Ion channel dysfunction in cerebellar ataxia.
Review in Neuroscience letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 76 citations in OpenAlex.
- Neuroprotection Across Cerebellar and Nigrostriatal Degeneration: Translational Insights from Parkinson's Disease to Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Review
- Functional and structural basis of a hypermorphic TRPC3 variant.Science advances · 2026Article
- A Novel Mouse Model for Developmental and Epileptic Encephalopathy by Purkinje Cell-Specific Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Autonomous STING signaling in Purkinje cells drives neurodegeneration independent of type I interferon.Cell reports · 2025Article
- Restoration of Shal/KCellular and molecular life sciences : CMLS · 2025Article
- Dysregulation of alternative splicing is a transcriptomic feature of patient-derived fibroblasts from CAG repeat expansion spinocerebellar ataxias.Human molecular genetics · 2025Article
- Genetic mechanisms of dynamic functional connectivity density in diabetic retinopathy brains: a combined transcriptomic and resting-state functional magnetic resonance imaging study.Frontiers in cellular neuroscience · 2025Article
- Dysregulation of zebrin-II cell subtypes in the cerebellum is a shared feature across polyglutamine ataxia mouse models and patients.Science translational medicine · 2024Article
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- Potential Benefit of Channel Activators in Loss-of-Function Primary Potassium Channelopathies Causing Heredoataxia.Cerebellum (London, England) · 2024Review
- Review
- Widespread alternative splicing dysregulation occurs presymptomatically in CAG expansion spinocerebellar ataxias.Brain : a journal of neurology · 2024Article
- Spinocerebellar ataxias: from pathogenesis to recent therapeutic advances.Frontiers in neuroscience · 2024Review
- Myoclonus and Dystonia as Recurrent Presenting Features in Patients with the SCA21-AssociatedTremor and other hyperkinetic movements (New York, N.Y.) · 2024Review
- Oxidative stress and ion channels in neurodegenerative diseases.Frontiers in physiology · 2024Review
- Clinical and electrophysiological features of SCN8A variants causing episodic or chronic ataxia.EBioMedicine · 2023Article
- Targeting Ion Channels and Purkinje Neuron Intrinsic Membrane Excitability as a Therapeutic Strategy for Cerebellar Ataxia.Life (Basel, Switzerland) · 2023Review
- Purkinje-Enriched snRNA-seq in SCA7 Cerebellum Reveals Zebrin Identity Loss as a Central Feature of Polyglutamine Ataxias.bioRxiv : the preprint server for biology · 2023Article
- What Is the Role of Norepinephrine in Cerebellar Modulation and Stress-Induced Episodic Ataxia?Neurology · 2023Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cerebellar ataxias constitute a heterogeneous group of disorders that result in impaired speech, uncoordinated limb movements, and impaired balance, often ultimately resulting in wheelchair confinement. Motor dysfunction in ataxia can be attributed to dysfunction and degeneration of neurons in the cerebellum and its associated pathways. Recent work has suggested the importance of cerebellar neuronal dysfunction resulting from mutations in specific ion-channels that regulate membrane excitability in the pathogenesis of cerebellar ataxia in humans. Importantly, even in ataxias not directly due to ion-channel mutations, transcriptional changes resulting in ion-channel dysfunction are tied to motor dysfunction and degeneration in models of disease. In this review, we describe the role that ion-channel dysfunction plays in a variety of cerebellar ataxias, and postulate that a potential therapeutic strategy that targets specific ion-channels exists for cerebellar ataxia.
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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.