ReviewAntioxidants (Basel, Switzerland)2021
Linking Oxidative Stress and Proteinopathy in Alzheimer's Disease.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Airborne pollutants and risk of neurodegenerative diseases: a global systematic review and meta-analysis.Alzheimer's research & therapy · 2026Pooled it
- Probiotics for Alzheimer's Disease: A Systematic Review.Nutrients · 2021Pooled it
- Targeting inflammaging in Alzheimer's disease: molecular pathways and emerging pharmacotherapies.Inflammopharmacology · 2026Review
- Isolation and identification of hasubanan alkaloids having anti-cholinesterase and antioxidant activity from the stem Stephania japonica.BMC complementary medicine and therapies · 2026Article
- Synthesis and Evaluation of Novel Cinnamic Acid Hybrids With Antiacetylcholinesterase, Antioxidant, and Anti-Inflammatory Properties.ChemMedChem · 2026Article
- Therapeutic Effects of miR-21-5p-Enriched Milk Extracellular Vesicles on Alzheimer's Disease-Associated Neurotoxicity in Vitro.Cell biochemistry and biophysics · 2026Article
- Sovateltide at the heart-brain axis crosstalk in Alzheimer's disease: a promising multi-target and cutting-edge therapeutic approach.Inflammopharmacology · 2026Review
- PAR-1 in Alzheimer's Disease: Pathophysiological Insights and Mechanistic Perspectives.Current medical science · 2026Review
- β-Alanine Is an Unexploited Neurotransmitter in the Pathogenesis and Treatment of Alzheimer's Disease.NeuroSci · 2026Review
- A Review on the Pathophysiology of Alzheimer's Disease.Current protein & peptide science · 2026Review
- Mitochondria as a Therapeutic Target in Neurodegeneration: Strategies for Restoring Cellular Homeostasis.Current neuropharmacology · 2026Review
- Therapeutic potential of vagus nerve stimulation in neurodegenerative diseases: research progress and mechanisms.Frontiers in immunology · 2026Review
- Association of Hemoglobin and Myoglobin into Supramolecular Complexes: Significance for Life and Practice.International journal of molecular sciences · 2025Review
- Mechanisms Underlying the Cognitive Benefits ofPlants (Basel, Switzerland) · 2025Article
- Development of Zebrafish model for Iron Induced Neuroinflammation.Fish physiology and biochemistry · 2025Article
- Ameliorative Role of Phosphodiesterase-5 (PDE-5) Inhibitor "Avanafil" via Modulating cAMP & cGMP Pathway Against Alzheimer's Disease.Neurochemical research · 2025Article
- Atractylenolide III alleviates amyloid-β-induced cognitive impairments in mice.Molecular biology reports · 2025Article
- The Redox Revolution in Brain Medicine: Targeting Oxidative Stress with AI, Multi-Omics and Mitochondrial Therapies for the Precision Eradication of Neurodegeneration.International journal of molecular sciences · 2025Review
- Korean black ginseng extract alleviates Alzheimer's disease-related cognitive impairment by activating the Nrf2/HO-1 pathway and suppressing the p38 MAPK/NF-κB/STAT3 pathways and NLRP3 inflammasome via TLR2 and TLR4 modulation.Journal of ginseng research · 2025Article
- Network pharmacology and metabolomics analysis of Tinospora cordifolia reveals BACE1 and MAOB as potential therapeutic targets for neuroprotection in Alzheimer's disease.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Proteinopathy and excessive production of reactive oxygen species (ROS), which are the principal features observed in the Alzheimer's disease (AD) brain, contribute to neuronal toxicity. β-amyloid and tau are the primary proteins responsible for the proteinopathy (amyloidopathy and tauopathy, respectively) in AD, which depends on ROS production; these aggregates can also generate ROS. These mechanisms work in concert and reinforce each other to drive the pathology observed in the aging brain, which primarily involves oxidative stress (OS). This, in turn, triggers neurodegeneration due to the subsequent loss of synapses and neurons. Understanding these interactions may thus aid in the identification of potential neuroprotective therapies that could be clinically useful. Here, we review the role of β-amyloid and tau in the activation of ROS production. We then further discuss how free radicals can influence structural changes in key toxic intermediates and describe the putative mechanisms by which OS and oligomers cause neuronal death.
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Registered trials
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