Evidence map›Paper›PMID 39754245›Full record

ArticleJournal of neuroinflammation2025

Complement inhibition targets a rich-club within the neuroinflammatory network after stroke to improve radiographic and functional outcomes.

Youssef M Zohdy, Tomas Garzon-Muvdi, Jonathan A Grossberg, Daniel L Barrow, Brian M Howard, Gustavo Pradilla, Firas H Kobeissy, Stephen Tomlinson, Ali M Alawieh

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Tracing Inflammation in Ischemic Stroke: Biomarkers and Clinical Insight.International journal of molecular sciences · 2025
    Review
  4. Review
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

9 authors.

Youssef M ZohdyDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Tomas Garzon-MuvdiDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Jonathan A GrossbergDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Daniel L BarrowDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Brian M HowardDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Gustavo PradillaDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Firas H KobeissyDepartment of Neurobiology, Morehouse School of Medicine, Atlanta, GA, USA.
Stephen TomlinsonDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.
Ali M AlawiehDepartment of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA. ali.mostafa.alawieh@emory.edu.

Funding

American Heart Association Fellowship Grant 15PRE25250009BLRD VA IK6 BX005235Department of Veterans Affairs Merit Awards 1BX004256Department of Veterans Affairs Merit Awards 1RX001141Department of Veterans Affairs Merit Awards 21RX002363Department of Veterans Affairs Merit Awards IK6BX005235
6 · The paper itself

Abstract

Following recent advances in post-thrombectomy stroke care, the role of neuroinflammation and neuroprotective strategies in mitigating secondary injury has gained prominence. Yet, while neuroprotection and anti-inflammatory agents have re-emerged in clinical trials, their success has been limited. The neuroinflammatory response in cerebral ischemia is robust and multifactorial, complicating therapeutic approaches targeting single pathways. In this study, we aimed to characterize early inflammatory gene dysregulation following ischemic stroke using translational in-silico and in-vivo approaches. Using an in vivo ischemic stroke model, transcriptomic analysis revealed significant dysregulation of inflammatory genes. Graph theory analysis then showed a rich-club organization among stroke-related genes, with highly connected core nodes. The expression levels of the core genes identified within this network significantly explained radiological outcomes, including T2-signal hyperintensity (R

Indexed as

Neuroinflammatory DiseasesAnimalsComplement Inactivating AgentsIschemic StrokeMaleMiceRatsRecovery of FunctionStrokeTreatment OutcomeComplement Inactivating AgentsComplement inhibitionNetwork analysisRich-clubStrokeTranscriptomics

Identifiers

PMID39754245
PMCPMC11699776

What OpenQuestion holds

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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.