ReviewNature reviews. Neuroscience2017
Polyglutamine spinocerebellar ataxias - from genes to potential treatments.
Review in Nature reviews. Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03487367 (Clinical Trial Readiness for SCA1 and SCA3), which is not on this map. Cited by 205 papers, 3 of them syntheses that pooled it.
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.
Clinical Trial Readiness for SCA1 and SCA3
Who cites it
205 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Quantitative Ocular Motor / Vestibular Assessment in Patients with Spinocerebellar Ataxia Type 3 (SCA3, Machado Joseph Disease) - Systematic Review of the Literature.Cerebellum (London, England) · 2026Pooled it
- Epidemiology of Spinocerebellar Ataxias in Europe.Cerebellum (London, England) · 2024Pooled it
- Pooled it
- Juvenile Huntington Disease With Cerebellar-Predominant Atrophy Identified by Genome Sequencing.Annals of clinical and translational neurology · 2026Article
- Beyond the brain: Polyglutamine disease pathology outside the nervous system.Neurobiology of disease · 2026Review
- Article
- Domain-dependent uncoupling of the co-chaperone and E3 ubiquitin ligase CHIP underlies heterogeneity in spinocerebellar ataxia 48.The Journal of biological chemistry · 2026Article
- Spinocerebellar Ataxia Type 3 Accompanied by Amyotrophic Lateral Sclerosis: A Case Report and Comprehensive Literature Review.Internal medicine (Tokyo, Japan) · 2026Review
- Improving the Identification of the Preclinical Stages of Spinocerebellar Ataxia Type 2.Tomography (Ann Arbor, Mich.) · 2026Article
- Targeting UCHL3 attenuates pathological markers in neuronal models of Huntington's disease.Brain : a journal of neurology · 2026Article
- Oxidative stress causes a reversible decrease of deubiquitylases activity in old vertebrate brains.Nature communications · 2026Article
- [Trinucleotide repeat disorders].Radiologie (Heidelberg, Germany) · 2026Review
- Experimental Models to Study Polyglutamine Spinocerebellar Ataxias: From Mechanisms to Therapeutic Developments.Cerebellum (London, England) · 2026Review
- Selective silencing of expanded CAG repeats: Chemically modified siRNA advances RNA-based therapies for polyglutamine diseases.Molecular therapy. Nucleic acids · 2026Article
- Expanding the Genetic Landscape ofNeurology. Genetics · 2026Article
- Repeat-associated non-AUG translation as a common mechanism for the polyGln ataxias.Cell reports · 2026Article
- Recreating the human brain: Are assembloids merely descriptive models?Frontiers in cellular neuroscience · 2026Review
- The Status and Future Directions of Treatments for Polyglutamine Spinocerebellar Ataxia: A Bibliometric and Visual Analysis.Current neuropharmacology · 2026Review
- Regional brain atrophy subtypes in spinocerebellar ataxia type 3: links to clinical performance and treatment response.Journal of neurology · 2025Article
- Practice Recommendations for Genetic Testing of Ataxias.Annals of clinical and translational neurology · 2025Review
145 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The dominantly inherited spinocerebellar ataxias (SCAs) are a large and diverse group of neurodegenerative diseases. The most prevalent SCAs (SCA1, SCA2, SCA3, SCA6 and SCA7) are caused by expansion of a glutamine-encoding CAG repeat in the affected gene. These SCAs represent a substantial portion of the polyglutamine neurodegenerative disorders and provide insight into this class of diseases as a whole. Recent years have seen considerable progress in deciphering the clinical, pathological, physiological and molecular aspects of the polyglutamine SCAs, with these advances establishing a solid base from which to pursue potential therapeutic approaches.
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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.