Evidence map›Paper›PMID 38923318›Full record

ArticlePhysiological reports2024

Chronic consequences of ischemic stroke: Profiling brain injury and inflammation in a mouse model with reperfusion.

Devin P Murphy, Denali C Dickson, Arisha N Fatema, Nolan G Carrasco, Kristian P Doyle, Theodore P Trouard, Helena W Morrison

Abstract read
In one paragraph

Article in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. 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

7 authors.

Devin P MurphyDepartment of Biomedical Engineering, College of Engineering, University of Arizona, Tucson, Arizona, USA.
Denali C DicksonCollege of Nursing, University of Arizona, Tucson, Arizona, USA.
Arisha N FatemaDepartment of Biomedical Engineering, College of Engineering, University of Arizona, Tucson, Arizona, USA.
Nolan G CarrascoCollege of Pharmacy, University of Arizona, Tucson, Arizona, USA.
Kristian P DoyleDepartment of Immunology, College of Medicine, University of Arizona, Tucson, Arizona, USA.
Theodore P TrouardDepartment of Biomedical Engineering, College of Engineering, University of Arizona, Tucson, Arizona, USA.
Helena W MorrisonCollege of Nursing, University of Arizona, Tucson, Arizona, USA.ORCID 0000-0003-3791-0190

Funding

Research Education ComponentP30AG072980 · NIA · BANNER HEALTH · PI ALIREZA ATRI · 2021 to 2026
$24.9M
Translational Research in Alzheimer's Disease and related Dementias (TRADD)T32AG082631 · NIA · UNIVERSITY OF ARIZONA · PI ROBERTA EILEEN BRINTON · 2023 to 2026
$1.2M
NanO2 as a Cerebroprotectant in a tMCAO Stroke Model in MiceR41NS124450 · NINDS · NUVOX PHARMA, LLC · PI MORRISON, HELENA WILLINGTON, UNGER, EVAN CHARLES · 2021 to 2021
$478k
NIA NIH HHS P30 AG072980NIA NIH HHS T32 AG082631NIA NIH HHS T32AG082631-01NINDS NIH HHS 1R41NS124450NINDS NIH HHS R41 NS124450
6 · The paper itself

Abstract

Stroke is a pervasive and debilitating global health concern, necessitating innovative therapeutic strategies, especially during recovery. While existing literature often focuses on acute interventions, our study addresses the uniqueness of brain tissue during wound healing, emphasizing the chronic phase following the commonly used middle cerebral artery (MCA) occlusion model. Using clinically relevant endpoints in male and female mice such as magnetic resonance imaging (MRI) and plasma neurofilament light (NFL) measurement, along with immunohistochemistry, we describe injury evolution. Our findings document significant alterations in edema, tissue remodeling, and gadolinium leakage through MRI. Plasma NFL concentration remained elevated at 30 days poststroke. Microglia responses are confined to the region adjacent to the injury, rather than continued widespread activation, and boron-dipyrromethene (BODIPY) staining demonstrated the persistent presence of foam cells within the infarct. Additional immunohistochemistry highlighted sustained B and T lymphocyte presence in the poststroke brain. These observations underscore potentially pivotal roles played by chronic inflammation brought on by the lipid-rich brain environment, and chronic blood-brain barrier dysfunction, in the development of secondary neurodegeneration. This study sheds light on the enduring consequences of ischemic stroke in the most used rodent stroke model and provides valuable insights for future research, clinical strategies, and therapeutic development.

Indexed as

Ischemic StrokeMice, Inbred C57BLAnimalsBlood-Brain BarrierBrainDisease Models, AnimalFemaleInfarction, Middle Cerebral ArteryInflammationMagnetic Resonance ImagingMaleMiceNeurofilament ProteinsReperfusion Injuryneurofilament protein LNeurofilament Proteinsblood–brain barrierchronic injuryfoam cellsischemic stroke

Identifiers

PMID38923318
PMCPMC11194179

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.