ReviewExperimental neurology2012
Redox regulation of protein misfolding, mitochondrial dysfunction, synaptic damage, and cell death in neurodegenerative diseases.
Review in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 114 citations in OpenAlex.
- Decode the Ubiquitinome in Parkinson's Disease: From Pathological Aggregates to Targeted DUB Therapeutics.Neuroscience bulletin · 2026Review
- Mitochondrial dysfunction and programmed cell death in Alzheimer's disease: A retrospective bioinformatics study.Medicine · 2026Article
- Aberrant Protein S-Nitrosylation Mimics the Effect of Rare Genetic Mutations in Neurodegenerative Diseases.Journal of neurochemistry · 2026Review
- A Blood-Brain Barrier-Penetrant Ag(III) Corrole Compound Rescues Alzheimer's Disease Pathology by Targeting Aβ42-Induced Oxidative Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cocaine affects astrocyte iNOS expression.Brain research · 2026Article
- Inhibition of iNOS reduced cerebral vasoconstriction from chronic cocaine and enhanced angiogenesis in the prefrontal cortex.Brain research bulletin · 2025Article
- Oxidative/Nitrosative Stress, Apoptosis, and Redox Signaling: Key Players in Neurodegenerative Diseases.Journal of biochemical and molecular toxicology · 2025Review
- Protein Oxidation in Aging and Alzheimer's Disease Brain.Antioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle.Frontiers in cell and developmental biology · 2024Article
- A review of experimental and clinical studies on the therapeutic effects of pomegranate (Food science & nutrition · 2023Review
- Review
- Review
- Review
- Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperoneAutophagy · 2021Article
- Aging-Dependent Mitophagy Dysfunction in Alzheimer's Disease.Molecular neurobiology · 2021Review
- Chinese nutraceuticals and physical activity; their role in neurodegenerative tauopathies.Chinese medicine · 2021Review
- Two genomes, one cell: Mitochondrial-nuclear coordination via epigenetic pathways.Molecular metabolism · 2020Review
- Amyloid aggregates of the deubiquitinase OTUB1 are neurotoxic, suggesting that they contribute to the development of Parkinson's disease.The Journal of biological chemistry · 2020Article
- NADExperimental neurology · 2020Review
- Allicin ameliorates obesity comorbid depressive-like behaviors: involvement of the oxidative stress, mitochondrial function, autophagy, insulin resistance and NOX/Nrf2 imbalance in mice.Metabolic brain disease · 2019Article
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 2 countries.
Funding
Abstract
The loss or injury of neurons associated with oxidative and nitrosative redox stress plays an important role in the onset of various neurodegenerative diseases. Specifically, nitric oxide (NO), can affect neuronal survival through a process called S-nitrosylation, by which the NO group undergoes a redox reaction with specific protein thiols. This in turn can lead to the accumulation of misfolded proteins, which generally form aggregates in Alzheimer's, Parkinson's, and other neurodegenerative diseases. Evidence suggests that S-nitrosylation can also impair mitochondrial function and lead to excessive fission of mitochondria and consequent bioenergetic compromise via effects on the activity of the fission protein dynamin-related protein 1 (Drp1). This insult leads to synaptic dysfunction and loss. Additionally, high levels of NO can S-nitrosylate a number of aberrant targets involved in neuronal survival pathways, including the antiapoptotic protein XIAP, inhibiting its ability to prevent apoptosis.
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.