ArticleOxidative medicine and cellular longevity2021
Redox Imbalance Associates with Clinical Worsening in Spinocerebellar Ataxia Type 2.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Neuroprotection Across Cerebellar and Nigrostriatal Degeneration: Translational Insights from Parkinson's Disease to Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Review
- Blood Glucose Homeostasis is Preserved in Patients with Mild-to-moderate Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Article
- Multiomics approach identifies SERPINB1 as candidate biomarker for spinocerebellar ataxia type 2.Scientific reports · 2025Article
- Biomarkers in Spinocerebellar Ataxias.Cerebellum (London, England) · 2025Review
- A comprehensive review of iPS cell line-based disease modelling of the polyglutamine spinocerebellar ataxias 2 and 3: a focus on the research outcomes.Annals of medicine and surgery (2012) · 2024Review
- Naturally Occurring Antioxidant Therapy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinocerebellar ataxia type 2 (SCA2) is a neurodegenerative disease presenting with redox imbalance. However, the nature and implications of redox imbalance in SCA2 physiopathology have not been fully understood.
objectiveThe objective of this study is to assess the redox imbalance and its association with disease severity in SCA2 mutation carriers.
methodsA case-control study was conducted involving molecularly confirmed SCA2 patients, presymptomatic individuals, and healthy controls. Several antioxidant parameters were assessed, including serum thiol concentration and the superoxide dismutase, catalase, and glutathione S-transferase enzymatic activities. Also, several prooxidant parameters were evaluated, including thiobarbituric acid-reactive species and protein carbonyl concentrations. Damage, protective, and OXY scores were computed. Clinical correlates were established.
resultsSignificant differences were found between comparison groups for redox markers, including protein carbonyl concentration (
conclusionsThere is a disruption of redox balance in SCA2 mutation carriers which depends on the disease stage. Besides, redox changes associate with markers of disease severity, suggesting a link between disruption of redox balance and SCA2 physiopathology.
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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.