ReviewLife (Basel, Switzerland)2020
Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration.
Review in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 116 citations in OpenAlex.
- An open label, non-randomized study assessing a prebiotic fiber intervention in a small cohort of Parkinson's disease participants.Nature communications · 2023Trial
- Oxidative Stress and Its Mitigation in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2026Article
- Review
- Exploring the neuroprotective, antioxidant, and anti-amyloid effects of Ganoderma lucidum compounds in Alzheimer's disease: insights from experimental and computational approaches.Journal, genetic engineering & biotechnology · 2026Article
- Stem Cell-Derived Extracellular Vesicles Ameliorate the Neuron Mitochondrial Damage Induced by ROS-, LPS-Exposure: In Vitro Model of Neuron, Microglia, and Astrocyte Triple Co-Culture.International journal of molecular sciences · 2026Article
- PHOX2B defects alter protein folding, cell-cycle, and mitochondrial pathways in an in vitro model of CCHS.Molecular medicine (Cambridge, Mass.) · 2026Article
- Copper Overload Affects α-Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model.Advanced biology · 2026Article
- Global Research Trends and Hotspots in Gene Editing and Stem Cell Therapies for Neurodegenerative Diseases: Bibliometric and Visualization Analysis.Interactive journal of medical research · 2026Review
- Modulation of the Kynurenine Pathway: A New Approach for Treating Neurodegeneration.Life (Basel, Switzerland) · 2026Review
- Review
- High-Frequency, Low-Intensity Pulsed Electric Field and N-Acetylcysteine Synergistically Protect SH-SY5Y Cells Against Hydrogen Peroxide-Induced Cell Damage In Vitro.Antioxidants (Basel, Switzerland) · 2025Article
- Decoding natural products for neuroprotection: Pathway networks and structural insights for drug development.Chinese herbal medicines · 2025Review
- AI-Enhanced Transcriptomic Discovery of Druggable Targets and Repurposed Therapies for Huntington's Disease.Brain sciences · 2025Review
- Secondary Metabolite Profiling ofLife (Basel, Switzerland) · 2025Article
- Short-Term Inhibition of NOX2 Prevents the Development of Aβ-Induced Pathology in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Signaling Pathways in Oxidative Stress-Induced Neurodegenerative Diseases: A Review of Phytochemical Therapeutic Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Protein Misfolding and Aggregation as a Mechanistic Link Between Chronic Pain and Neurodegenerative Diseases.Current issues in molecular biology · 2025Review
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Pro-Oxidative and Inflammatory Actions of Extracellular Hemoglobin and Heme: Molecular Events and Implications for Alzheimer's and Parkinson Disease.Biomolecules & therapeutics · 2025Review
- Advances in Molecular Docking Techniques for Targeting Protein Misfolding in Neurodegenerative Diseases.Current pharmaceutical biotechnology · 2025Review
8 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 at 3 institutions in 2 countries.
Funding
Abstract
Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones-Alzheimer's and Parkinson's disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.
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.