ArticleNeurochemical research2009
Glutathionylation of the pro-apoptotic protein p53 in Alzheimer's disease brain: implications for AD pathogenesis.
Article in Neurochemical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 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
41 citing papers in PubMed, 77 citations in OpenAlex.
- Clinical insights into catechin-based nanomedicine: a review of therapeutic potential in neurodegenerative diseases.3 Biotech · 2025Review
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- Review
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- Defining the S-Glutathionylation Proteome by Biochemical and Mass Spectrometric Approaches.Antioxidants (Basel, Switzerland) · 2022Review
- Catechins as a Potential Dietary Supplementation in Prevention of Comorbidities Linked with Down Syndrome.Nutrients · 2022Review
- Aging, Cellular Senescence, and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Metabolic Features of Brain Function with Relevance to Clinical Features of Alzheimer and Parkinson Diseases.Molecules (Basel, Switzerland) · 2022Review
- Anti-Oxidative, Anti-Inflammatory and Anti-Apoptotic Effects of Flavonols: Targeting Nrf2, NF-κB and p53 Pathways in Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Redox Regulation by Protein S-Glutathionylation: From Molecular Mechanisms to Implications in Health and Disease.International journal of molecular sciences · 2020Review
- Design, Synthesis, and Evaluation of Acetylcholinesterase and Butyrylcholinesterase Dual-Target Inhibitors against Alzheimer's Diseases.Molecules (Basel, Switzerland) · 2020Article
- Effects of Smoking on Regional Homogeneity in Mild Cognitive Impairment: A Resting-State Functional MRI Study.Frontiers in aging neuroscience · 2020Article
- Autophagy and Redox Homeostasis in Parkinson's: A Crucial Balancing Act.Oxidative medicine and cellular longevity · 2020Review
- Phosphoproteomics of Alzheimer disease brain: Insights into altered brain protein regulation of critical neuronal functions and their contributions to subsequent cognitive loss.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- p53 as a hub in cellular redox regulation and therapeutic target in cancer.Journal of molecular cell biology · 2019Review
- The intact postsynaptic protein neurogranin is reduced in brain tissue from patients with familial and sporadic Alzheimer's disease.Acta neuropathologica · 2019Article
- The roles of S-nitrosylation and S-glutathionylation in Alzheimer's disease.Methods in enzymology · 2019Review
- Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2018Review
- Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.Antioxidants & redox signaling · 2017Review
Corrections and comments
- Erratum issuedD Domenico, Fabio [corrected to Di Domenico, Fabio]
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. The exact mechanism for the AD pathogenesis is not clearly understood. However, a number of hypotheses have been proposed to explain the pathogenesis of AD. One the hypotheses is the oxidative stress hypothesis that is supported by a number of studies which reported an increase in the levels of reactive oxygen/reactive nitrogen species and their products with a concomitant decrease in the levels of antioxidant enzymes in AD brain. In the present study, we measured in AD brain the expression levels of different forms (monomer, dimer and tetramer) of the pro-apoptotic protein, p53, and observed greater levels of p53 monomer and dimer in AD brain compared to control. In addition, we also showed the selective glutathionylation of monomeric and dimeric form of p53 in AD brain. We propose that glutathionylation of p53 may prevent the formation of tetramer, an aggregate form required for effective action of p53, and may be involved in oxidative stress conditions and neurodegeneration observed in this dementing disorder.
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.