ReviewCerebellum (London, England)2008
Spinocerebellar ataxia 2 (SCA2).
Review in Cerebellum (London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 197 citations in OpenAlex.
- Magnetic resonance imaging for spinocerebellar ataxia: a bibliometric analysis based on web of science.Frontiers in neurology · 2025Pooled it
- Amyotrophic lateral sclerosis risk for spinocerebellar ataxia type 2 ATXN2 CAG repeat alleles: a meta-analysis.JAMA neurology · 2014Pooled it
- Article
- Bioinformatic Analyses of the Ataxin-2 Family Since Algae Emphasize Its Small Isoforms, Large Chimerisms, and the Importance of Human Exon 1B as Target of Therapies to Prevent Neurodegeneration.International journal of molecular sciences · 2026Article
- Expanding the Genetic Landscape ofNeurology. Genetics · 2026Article
- Article
- Influence of ATXN2 intermediate CAG repeats, 9bp duplication and alternative splicing on SCA3 pathogenesis.Acta neuropathologica communications · 2025Article
- Three Cases of Spinocerebellar Ataxia Type 2 (SCA2) and Pediatric Literature Review: Do Not Forget Trinucleotide Repeat Disorders in Childhood-Onset Progressive Ataxia.Brain sciences · 2025Article
- Post-symptomatic administration of hMSCs exerts therapeutic effects in SCA2 mice.Stem cell research & therapy · 2024Article
- Ataxin-2: a powerful RNA-binding protein.Discover oncology · 2024Review
- Fatigue Impacts Quality of Life in People with Spinocerebellar Ataxias.Movement disorders clinical practice · 2024Article
- MRl and MRS hints for the differentiation of cerebellar multiple system atrophy from spinocerebellar ataxia type II.Heliyon · 2024Article
- Intermediate Repeat Expansion in theBiomedicines · 2024Article
- TDP-43 impairs sleep inScience advances · 2024Article
- In Vivo Validation of a Mechanically Adaptive Microfluidic Intracortical Device as a Platform for Sustained Local Drug Delivery.Frontiers in biomaterials science · 2023Article
- ATXN2 is a target of N-terminal proteolysis.PloS one · 2023Article
- Recent progress of the genetics of amyotrophic lateral sclerosis and challenges of gene therapy.Frontiers in neuroscience · 2023Review
- Review
- Structure-Activity Relationship Study of Subtype-Selective Positive Modulators of KJournal of medicinal chemistry · 2022Article
- A C-terminal ataxin-2 disordered region promotes Huntingtin protein aggregation and neurodegeneration in Drosophila models of Huntington's disease.G3 (Bethesda, Md.) · 2021Article
53 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominantly inherited, neurodegenerative disease. It can manifest either with a cerebellar syndrome or as Parkinson's syndrome, while later stages involve mainly brainstem, spinal cord and thalamus. This particular atrophy pattern resembles sporadic multi-system-atrophy (MSA) and results in some clinical features indicative of SCA2, such as early saccade slowing, early hyporeflexia, severe tremor of postural or action type, and early myoclonus. For treatment, levodopa is temporarily useful for rigidity/bradykinesia and for tremor, magnesium for muscle cramps, but neuroprotective therapy will depend on the elucidation of pathogenesis. The disease cause lies in the polyglutamine domain of the protein ataxin-2, which can expand in families over successive generations resulting in earlier onset age and faster progression. Genetic testing in SCA2 and other polyglutamine disorders like the well-studied Huntington's disease is now readily available for family planning. Although these disorders differ clinically and in the affected neuron populations, it is not understood how the different polyglutamine proteins mediate such tissue specificity. The neuronal intranuclear inclusion bodies described in other polyglutamine disorders are not frequent in SCA2. For the quite ubiquitously expressed ataxin-2, a subcellular localization at the Golgi, the endoplasmic reticulum and the plasma membrane, in interaction with proteins of mRNA translation and of endocytosis have been observed. As a first victim of SCA2 degeneration, cerebellar Purkinje neurons may be preferentially susceptible to alterations of these subcellular pathways, and therefore our review aims to portray the particular profile of the SCA2 disease process and correlate it to the specific features of ataxin-2.
Indexed as
Identifiers
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.