Evidence map›Paper›PMID 39904881›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2025

TMEM119-positive microglial cells in cerebrospinal fluid, a potential new marker for neuroinflammatory response after aneurysmal subarachnoid hemorrhage.

Andrea Cattaneo, Julia Messinger, Kevin Lamllari, Helmut Heinsen, Michael K Schuhmann, Christoph Wipplinger, Vera Nickl, Mario Löhr, Ekkehard Kunze, Christian Stetter and 7 more

Abstract read
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Observational
  3. 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

17 authors.

Andrea CattaneoDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany. Cattaneo_A@ukw.de.
Julia MessingerDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Kevin LamllariDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Helmut HeinsenInstitute of Forensic Medicine, University of Würzburg, Würzburg, Germany.
Michael K SchuhmannDepartment of Neurology, University Hospital Würzburg, Würzburg, Germany.
Christoph WipplingerDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Vera NicklDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Mario LöhrDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Ekkehard KunzeDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Christian StetterDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Thomas LinsenmannDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Michael BohnertInstitute of Forensic Medicine, University of Würzburg, Würzburg, Germany.
Ralf-Ingo ErnestusDepartment of Neurosurgery, University Hospital of Würzburg, Würzburg, Germany.
Johann ZwirnerInstitute of Legal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Benjamin OndruschkaInstitute of Legal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Camelia-Maria MonoranuDepartment of Neuropathology, Institute of Pathology, University of Würzburg, Würzburg, Germany.ORCID 0000-0002-1345-7363
Simone BohnertInstitute of Forensic Medicine, University of Würzburg, Würzburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) is a debilitating condition with significant morbidity and mortality rates. Despite advancements in treatment, understanding the underlying pathophysiology, particularly the inflammatory response, remains crucial for improving patient outcomes. In this study, we investigated the presence of transmembrane protein 119 (TMEM119) of microglial cells in cerebrospinal fluid (CSF) as a potential marker for neuroinflammation following aSAH. CSF samples were collected from aSAH patients, pathological and healthy controls, processed, and analyzed using immunocytochemistry. TMEM119-positive microglial cells were consistently identified in the CSF of aSAH patients, exhibiting amoeboid morphology and intense staining. Importantly, microglial cells were detected as early as the first day post-bleeding, persisting throughout the acute phase in some cases. Analysis of consecutive samples revealed varying trends in microglial cell numbers, with a peak during the initial phase followed by a gradual decline. Our findings suggest that microglia may migrate into the CSF following aSAH, potentially serving as an early predictor of inflammatory-related CNS damage. This study underscores the importance of understanding neuroinflammatory processes in aSAH and opens avenues for further research on the role of microglia in CNS disorders by liquid biopsy.

Indexed as

Membrane ProteinsMicrogliaNeuroinflammatory DiseasesSubarachnoid HemorrhageAdultAgedBiomarkersFemaleHumansMaleMiddle AgedBiomarkersMembrane ProteinsTmem119 protein, humanCerebrospinal fluidInflammationMicrogliaSubarachnoid hemorrhageTMEM119

Identifiers

PMID39904881
PMCPMC12043730

What Socratic holds

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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 Socratic graph.