Evidence map›Paper›PMID 42479781›Full record

ArticleMacromolecular bioscience2026

Thiol-Based Neuroprotective Copolymers Acutely Restore Redox Metabolism and Mediate Vasogenic Edema in a Mouse Model of Traumatic Brain Injury.

Evan T Curtis, Brandon Z McDonald, Aria W Tarudji, Aaron M Priester, Anthony J Convertine, Forrest M Kievit

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Macromolecular bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Evan T CurtisDepartment of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Brandon Z McDonaldDepartment of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Aria W TarudjiDepartment of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Aaron M PriesterDepartment of Material Science and Engineering, Missouri University of Science and Technology, Rolla, Missouri, USA.
Anthony J ConvertineDepartment of Material Science and Engineering, Missouri University of Science and Technology, Rolla, Missouri, USA.
Forrest M KievitDepartment of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.ORCID https://orcid.org/0000-0002-9847-783X

Funding

Nanoparticle-mediated reduction of oxidative stress for the treatment of traumatic brain injuryR01NS109488 · NINDS · UNIVERSITY OF NEBRASKA LINCOLN · PI KIEVIT, FORREST M · 2019 to 2023
$2.2M
Molecular Mechanisms of DiseaseT32GM136593 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI Donald F Becker, EDWARD N HARRIS · 2020 to 2026
$1.8M
National Institute of Neurological Disorders and Stroke of the National Institutes of Health R01NS109488NIGMS NIH HHS T32 GM136593NINDS NIH HHS R01 NS109488
6 · The paper itself

Abstract

Effective pharmaceutical interventions for treating the secondary damage associated with traumatic brain injury (TBI) are limited due to poor delivery into the brain, insufficient target engagement, and an incomplete understanding of the pathophysiological changes that occur post-impact. Thus, nanoparticles (NP), which have an enhanced permeation and retention-like effect within the perturbed blood-brain barrier, have grown as a potential candidate for treating TBI. We have investigated the antioxidant capacity of thiol-based NP, termed neuroprotective copolymers (NPC3), and their ability to neutralize reactive oxygen species (ROS) and lipid peroxidation products (LPOx). Here, we assessed the efficacy of NPC3 for alleviating the secondary injury cascade in TBI with a specific focus on ameliorating molecular and structural deficits in a mouse controlled cortical impact (CCI) model. NPC3 delivered post-CCI alleviated oxidant burden, reducing both antioxidant enzyme expression and Nrf2 activation. These changes in redox signaling resulted in a shift in metabolic function, with increased AMPK activation with NPC3 treatment. T2-weighted and diffusion magnetic resonance imaging revealed vasogenic edema formation at 30 days post-CCI and alterations in mean diffusivity, which were moderated by NPC3. Furthermore, NPC3 reduced GFAP and Iba1 at multiple impact severities, which positively correlated with urinary 8-isoprostane. Overall, this work shows NPC3 reduced glial reactivity, affected redox metabolism, and ultimately contributed to improvements in structural deficits post-CCI.

Indexed as

Brain EdemaBrain Injuries, TraumaticNeuroprotective AgentsPolymersSulfhydryl CompoundsAnimalsAntioxidantsBlood-Brain BarrierDisease Models, AnimalGlial Fibrillary Acidic ProteinLipid PeroxidationMaleMiceMice, Inbred C57BLNanoparticlesNF-E2-Related Factor 2AntioxidantsGlial Fibrillary Acidic ProteinNeuroprotective AgentsNF-E2-Related Factor 2PolymersReactive Oxygen SpeciesSulfhydryl Compoundscellular metabolismnanoparticlesoxidative stresstraumatic brain injuryvasogenic edema

Identifiers

PMID42479781
PMCPMC13387508

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.