ReviewRedox report : communications in free radical research2026
Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator.
Review in Redox report : communications in free radical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo evaluate the central role of oxidative stress in neurodegenerative diseases, and to explore its dynamic regulatory features, underlying signaling pathways, and molecular mechanisms, as well as advanced technological strategies for antioxidant intervention.
methodsThis review comprehensively evaluated existing literature on oxidative stress in neurodegenerative diseases. It analyzed key regulatory pathways (Nrf2, Keap1, AMPK, mTOR) and molecular processes, including ferroptosis, NETosis, and mitochondrial quality control systems, along with oxidative damage to DNA, lipids, and proteins. The review also assessed advanced technological approaches such as subcellular organelle targeting, nanocarrier delivery systems (e.g. gold nanoparticles, liposomes for glutathione delivery), and single-cell/spatial omics technologies (e.g. single-cell redoxomics, spatial transcriptomics).
resultsOxidative stress exhibits dynamic features, generating protective signals in early stages but transitioning into destructive factors later. A major obstacle for current antioxidant therapies is the blood-brain barrier. Breakthrough strategies identified include precision targeting at the subcellular level, functionalized nanoparticles for efficient antioxidant delivery, and the integration of single-cell redoxomics with spatial transcriptomics to identify specific biomarkers and enable personalized treatments. DISCUSSION: By integrating novel molecular mechanisms and advanced technological resources, this review redefines oxidative stress not as a singular event but as a complex, dynamically regulated system in neurodegenerative diseases. This reconceptualization provides new perspectives for developing targeted and personalized therapeutic interventions.
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Identifiers
What Socratic 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 Socratic graph.