ReviewProgress in neurobiology2023
NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.
Review in Progress in neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Plasma proteomics implicates NOX-driven redox imbalance in degenerative cervical myelopathy: findings from the Australian MYelopathy Natural History Registry [AO Spine RECODE-DCM research priority number 5].Redox report : communications in free radical research · 2026Article
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Effects of Decabromodiphenyl Ether (BDE209) Exposure on Toxicity and Oxidative Stress of Beas-2B Cells.Toxics · 2025Article
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.Antioxidants (Basel, Switzerland) · 2025Review
- Chronic lipopolysaccharide exposure promotes cognitive impairments by activating TRPC6-AIM2 inflammasome signaling and the regulation of ginsenoside Rg1 in Trpc6Behavioral and brain functions : BBF · 2025Article
- Glutathione Decreases Parkinsonism-Induced Ferroptosis and Oxidative Stress Through the Inhibition of the TRPM2 Channel in Neuronal Cells.Pharmacology research & perspectives · 2025Article
- Short-Term Inhibition of NOX2 Prevents the Development of Aβ-Induced Pathology in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Reversible reduction in brain myelin content upon marathon running.Nature metabolism · 2025Observational
- Article
- From a traditional medicine monomer to a modern neurotherapeutic scaffold: a review of SAR-Driven tetramethylpyrazine derivatives for cerebrovascular and cognitive health.Frontiers in pharmacology · 2025Review
- Molecular Roles of NADPH Oxidase-Mediated Oxidative Stress in Alzheimer's Disease: Isoform-Specific Contributions.International journal of molecular sciences · 2024Review
- Review
- Redox Homeostasis, Gut Microbiota, and Epigenetics in Neurodegenerative Diseases: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Inositol Hexaphosphate as an Inhibitor and Potential Regulator of p47Biochemistry · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Neurodegenerative diseases (NDDs) causing cognitive impairment and dementia are difficult to treat due to the lack of understanding of primary initiating factors. Meanwhile, major sporadic NDDs share many risk factors and exhibit similar pathologies in their early stages, indicating the existence of common initiation pathways. Glucose hypometabolism associated with oxidative stress is one such primary, early and shared pathology, and a likely major cause of detrimental disease-associated cascades; targeting this common pathology may therefore be an effective preventative strategy for most sporadic NDDs. However, its exact cause and trigger remain unclear. Recent research suggests that early oxidative stress caused by NADPH oxidase (NOX) activation is a shared initiating mechanism among major sporadic NDDs and could prove to be the long-sought ubiquitous NDD trigger. We focus on two major NDDs - Alzheimer's disease (AD) and Parkinson's disease (PD), as well as on acquired epilepsy which is an increasingly recognized comorbidity in NDDs. We also discuss available data suggesting the relevance of the proposed mechanisms to other NDDs. We delve into the commonalities among these NDDs in neuroinflammation and NOX involvement to identify potential therapeutic targets and gain a deeper understanding of the underlying causes of NDDs.
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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 Socratic graph.