ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019
Genetics, Mechanisms, and Therapeutic Progress in Polyglutamine Spinocerebellar Ataxias.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 140 citations in OpenAlex.
- TandemTwister: scalable genotyping and advanced visualization of tandem repeats.NAR genomics and bioinformatics · 2026Article
- Domain-dependent uncoupling of the co-chaperone and E3 ubiquitin ligase CHIP underlies heterogeneity in spinocerebellar ataxia 48.The Journal of biological chemistry · 2026Article
- Autophagy at the Crossroads of Protein and RNA Toxicity in Repeat Expansion Cerebellar Ataxias.Cells · 2026Review
- Cerebellar cognitive affective syndrome (CCAS) and [18F]-FDG PET findings in spinocerebellar ataxia type SCA27B.Journal of neurology · 2026Article
- Experimental Models to Study Polyglutamine Spinocerebellar Ataxias: From Mechanisms to Therapeutic Developments.Cerebellum (London, England) · 2026Review
- Treatment of primary adult-onset neurodegenerative cerebellar ataxias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- The Status and Future Directions of Treatments for Polyglutamine Spinocerebellar Ataxia: A Bibliometric and Visual Analysis.Current neuropharmacology · 2026Review
- Oral KDS2010, a Monoamine Oxidase-B (MAO-B) Inhibitor, Slows the Deterioration of Motor Coordination in Genetic SCA1 Models by Inhibiting Astrocytic MAO-B-Mediated Inflammation.Journal of neurochemistry · 2025Article
- Molecular hallmarks of neurodegeneration in polyglutamine spinocerebellar ataxias.Cell death & disease · 2025Review
- Past, present, and future of genomic technologies in cerebellar ataxias.Journal of neurology · 2025Review
- Challenges in Polyglutamine Diseases: From Dysfunctional Neuronal Circuitries to Neuron-Specific CAG Repeat Instability.International journal of molecular sciences · 2025Review
- Progressive subcortical involvement as spinocerebellar ataxia type 3 advances.Orphanet journal of rare diseases · 2025Article
- Pathophysiological role of high mobility group box-1 signaling in neurodegenerative diseases.Inflammopharmacology · 2025Review
- Clinical and genetic analysis of a case series of 12 Chinese families with hereditary ataxia.Frontiers in neurology · 2025Article
- 7T magnetic resonance imaging-based investigation of the correlation between mammillary body structure and cognitive impairment in patients with spinocerebellar ataxia type 3.Psychoradiology · 2025Article
- Dietary and lifestyle interventions for the management of hereditary ataxias.Frontiers in nutrition · 2025Review
- Decoding the genetic blueprints of neurological disorders: disease mechanisms and breakthrough gene therapies.Frontiers in neurology · 2025Review
- Clinic vs. daily life gait characteristics in patients with spinocerebellar ataxia.Frontiers in digital health · 2025Article
- Natural compounds as therapeutic candidates for spinocerebellar ataxia type 1: a computational approach.In silico pharmacology · 2025Article
- Spinocerebellar Ataxia in Brazil: A Comprehensive Genotype - Phenotype Analysis.Cerebellum (London, England) · 2024Observational
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Autosomal dominant cerebellar ataxias (ADCAs) are a group of neurodegenerative disorders characterized by degeneration of the cerebellum and its connections. All ADCAs have progressive ataxia as their main clinical feature, frequently accompanied by dysarthria and oculomotor deficits. The most common spinocerebellar ataxias (SCAs) are 6 polyglutamine (polyQ) SCAs. These diseases are all caused by a CAG repeat expansion in the coding region of a gene. Currently, no curative treatment is available for any of the polyQ SCAs, but increasing knowledge on the genetics and the pathological mechanisms of these polyQ SCAs has provided promising therapeutic targets to potentially slow disease progression. Potential treatments can be divided into pharmacological and gene therapies that target the toxic downstream effects, gene therapies that target the polyQ SCA genes, and stem cell replacement therapies. Here, we will provide a review on the genetics, mechanisms, and therapeutic progress in polyglutamine spinocerebellar ataxias.
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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.