Evidence map›Paper›PMID 42762327›Full record

ArticleExperimental brain research2026

Repeated impacts induce acute neurobehavioral and molecular deficits in a mouse model of traumatic brain injury.

Brandon Z McDonald, Connor C Gee, Aria W Tarudji, Evan T Curtis, Forrest M Kievit

Abstract read
PubMed Publisher
In one paragraph

Article in Experimental brain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Brandon Z McDonaldDepartment of Biological Systems Engineering, University of Nebraska - Lincoln, 264 Morrison Center, 4240 Fair St., Lincoln, NE, 68583, USA.
Connor C GeeDepartment of Biological Systems Engineering, University of Nebraska - Lincoln, 264 Morrison Center, 4240 Fair St., Lincoln, NE, 68583, USA.
Aria W TarudjiDepartment of Biological Systems Engineering, University of Nebraska - Lincoln, 264 Morrison Center, 4240 Fair St., Lincoln, NE, 68583, USA.
Evan T CurtisDepartment of Biological Systems Engineering, University of Nebraska - Lincoln, 264 Morrison Center, 4240 Fair St., Lincoln, NE, 68583, USA.
Forrest M KievitDepartment of Biological Systems Engineering, University of Nebraska - Lincoln, 268 Morrison Center, 4240 Fair St., Lincoln, NE, 68583, USA. fkievit2@unl.edu.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
NIGMS NIH HHS T32GM136593NINDS NIH HHS R01NS109488
6 · The paper itself

Abstract

Redox stress is a significant contributor to the molecular dysfunction associated with traumatic brain injury (TBI). Each of the canonical molecular biomarkers of TBI, including GFAP and UCHL1, demonstrate a clear relationship with redox stress via protein oxidation and enzymatic inhibition. Additionally, several markers of redox stress have demonstrated utility in assessing preclinical and clinical TBI, including F2-isoprostanes, generated from the oxidation of arachidonic acid. Thus, we investigated the role of urinary 8-isoprostane as a biomarker for delineating between sham and impacted mice. In this study, male and female mice (n = 19) subjected to five daily impacts using a repeated impact acceleration (rIA) model were evaluated against sham mice for neurological deficits. Impacted mice exhibited behavioral deficits, with increases in righting reflex (RR) times (p < 0.0001), and time-course increases in modified neurological severity scores (mNSS) (p < 0.01). Urine collected immediately following (day 5) and 72 h post-rIA (day 8) revealed time-course increases in 8-isoprostane levels (p < 0.05). Tissue-based protein expression for several markers of molecular dysfunction was assessed using immunoblotting in a two stage discovery based strategy, for which GFAP expression significantly differed with respect to treatment (p < 0.0001) and sex (p < 0.01). Pooled, unadjusted analysis identified a significant relationship between GFAP and urinary 8-isoprostane levels at day 8 (R

Indexed as

Brain Injuries, TraumaticDinoprostAnimalsBiomarkersDisease Models, AnimalFemaleGlial Fibrillary Acidic ProteinMaleMiceMice, Inbred C57BLOxidative StressReflex, Righting8-epi-prostaglandin F2alphaBiomarkersDinoprostGlial Fibrillary Acidic ProteinArachidonic acidBiomarkersLipid peroxidation productRedox stress

Identifiers

PMID42762327

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.