ReviewAntioxidants (Basel, Switzerland)2020
ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease.
Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 581 papers, 2 of them syntheses that pooled it.
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
581 citing papers in PubMed, 2 syntheses or guidelines pooled it, 942 citations in OpenAlex.
- Environmental epigenetic modifiers in neurodegenerative diseases: a systematic review of epigenomic mechanisms and therapeutic targets.Frontiers in epigenetics and epigenomics · 2026Pooled it
- p-Cresol and p-Cresyl Sulphate Boost Oxidative Stress: A Systematic Review of Recent Evidence.Basic & clinical pharmacology & toxicology · 2025Pooled it
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Arbutin mediated neuroprotection in zebrafish model of traumatic brain injury via modulating Nrf2/NF-κB pathway.Inflammopharmacology · 2026Article
- Reprogramming the oxidative microenvironment: Antioxidant nanoplatforms for central nervous system repair.Materials today. Bio · 2026Review
- PLXDC2 siRNA-Mediated Intervention Attenuates Microglial Senescence Through cGAS-STING Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- GPCR-Driven Muscarinic M1 and Histamine H1 Receptor Signaling Converging on the PI3K/Akt/mTOR Pathway: Functional Integration in Neuroinflammation and Myelin Repair in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Erinacine C Attenuates Alzheimer's-like Pathology: A Study in APP/PS1 Mice and PC12 Cells.Molecules (Basel, Switzerland) · 2026Article
- Dysfunction of hippocampal cells and its role in cognitive impairment.Neural regeneration research · 2026Article
- Distinct Transcriptomic Signatures of HIV-1 Tat and gp120 Uncover Differential Neuroimmune Vulnerability in aCurrent issues in molecular biology · 2026Article
- Fibrinogen as a Driver of Oxidative Stress and Apoptosis in the Fetal Brain After Maternal Influenza.Research square · 2026Article
- Silymarin attenuates senescence-exacerbated amyloidogenesis, neuroinflammation, and oxidative stress in lipopolysaccharide-induced memory impairment in aging mice.Biogerontology · 2026Article
- Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson's disease.Metabolic brain disease · 2026Review
- TRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.Schizophrenia bulletin · 2026Article
- ATOX1 overexpression mitigates copper homeostasis in microglia: Implications for Alzheimer's disease therapy.Genes & diseases · 2026Article
- Targeting mitochondrial dysfunction and neuroprotection in neurodegenerative disorders: emerging therapeutic potential of berberine and polymeric nanoparticle-based delivery systems.Inflammopharmacology · 2026Review
- Rapid Metabolic and Behavioral Maladaptations Following Short-Term Obesogenic Diet Withdrawal During Postweaning Development in Male Wistar Rats.Brain and behavior · 2026Article
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
521 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegenerative disorders, such as Alzheimer's disease, are a global public health burden with poorly understood aetiology. Neuroinflammation and oxidative stress (OS) are undoubtedly hallmarks of neurodegeneration, contributing to disease progression. Protein aggregation and neuronal damage result in the activation of disease-associated microglia (DAM) via damage-associated molecular patterns (DAMPs). DAM facilitate persistent inflammation and reactive oxygen species (ROS) generation. However, the molecular mechanisms linking DAM activation and OS have not been well-defined; thus targeting these cells for clinical benefit has not been possible. In microglia, ROS are generated primarily by NADPH oxidase 2 (NOX2) and activation of NOX2 in DAM is associated with DAMP signalling, inflammation and amyloid plaque deposition, especially in the cerebrovasculature. Additionally, ROS originating from both NOX and the mitochondria may act as second messengers to propagate immune activation; thus intracellular ROS signalling may underlie excessive inflammation and OS. Targeting key kinases in the inflammatory response could cease inflammation and promote tissue repair. Expression of antioxidant proteins in microglia, such as NADPH dehydrogenase 1 (NQO1), is promoted by transcription factor Nrf2, which functions to control inflammation and limit OS. Lipid droplet accumulating microglia (LDAM) may also represent a double-edged sword in neurodegenerative disease by sequestering peroxidised lipids in non-pathological ageing but becoming dysregulated and pro-inflammatory in disease. We suggest that future studies should focus on targeted manipulation of NOX in the microglia to understand the molecular mechanisms driving inflammatory-related NOX activation. Finally, we discuss recent evidence that therapeutic target identification should be unbiased and founded on relevant pathophysiological assays to facilitate the discovery of translatable antioxidant and anti-inflammatory therapeutics.
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.