ReviewCNS neuroscience & therapeutics2026
Stem Cell and EV/sEV Strategies for Neuroimmune Niche Reprogramming in Selected CNS Disorders: Mechanisms, Engineered Delivery, and Translational Readiness.
Review in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
Abstract
backgroundAging has traditionally been interpreted through the accumulation of oxidative damage. However, reactive oxygen species (ROS) also act as regulated signals that support immune activation, metabolic adaptation, stress resistance, inflammatory resolution, and cell-fate decisions. We define redox signaling fidelity as the accuracy with which a specified physiological input is converted into a source-specific, spatially confined, temporally patterned, chemically reversible, proportionately decoded, and appropriately resolved redox response.
methodsThis critical narrative review develops redox signaling fidelity as a testable systems framework rather than as a synonym for oxidative stress, redox homeostasis, oxidative eustress, hormesis, the redox code, or Redox-stress Response Capacity. The framework organizes redox information flow into five linked layers: generation, encoding, transmission, decoding, and resolution/reset. Aging may lower fidelity through source uncoupling, persistent cysteine oxidation, microdomain leakage, decoder bias, and defective autophagic, mitophagic, lysosomal, or proteostatic reset. Immune aging and the aging brain are used as cross-scale test cases in which physiological ROS pulses must be distinguished from chronic redox noise. We propose operational readouts, including source coupling, redox signal-to-noise ratio, reversibility, spatial leakage, decoder proportionality, mutual information, and resolution kinetics, and map these readouts to single-cell imaging, redox proteomics, spatial and single-cell omics, and dynamic modeling.
conclusionsThe fidelity framework predicts that lowering bulk ROS is not sufficient to restore redox function. More decisive studies should pair controlled inputs with compartment-resolved redox dynamics, reversible molecular encoding, pathway output, and functional recovery in the same young-versus-aged system. Interventions should be evaluated by whether they reduce pathological redox noise while preserving physiological pulses, spatial routing, adaptive decoding, and timely resolution.
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.