Evidence map›Paper›PMID 37521293›Full record

ArticleFrontiers in neurology2023

Neuropathology in COVID-19 autopsies is defined by microglial activation and lesions of the white matter with emphasis in cerebellar and brain stem areas.

Julian A Stein, Manuel Kaes, Sigrun Smola, Walter J Schulz-Schaeffer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Human brain matters: Navigating the neuropathology of COVID-19.Brain pathology (Zurich, Switzerland) · 2026
    Review
  2. Task-Evoked Pupillary Dynamics Are Altered in Post-COVID Syndrome.Medical sciences (Basel, Switzerland) · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Neuroimmune pathophysiology of long COVID.Psychiatry and clinical neurosciences · 2025
    Review
  8. Reemerging Infectious Diseases and Neuroimmunologic Complications.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. 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

4 authors at 2 institutions in 1 country.

Julian A SteinInstitute of Neuropathology, Medical Faculty of the Saarland University, Homburg, Germany.
Manuel KaesInstitute of Neuropathology, Medical Faculty of the Saarland University, Homburg, Germany.
Sigrun SmolaInstitute of Virology, Saarland University Medical Center, Homburg, Germany.
Walter J Schulz-SchaefferInstitute of Neuropathology, Medical Faculty of the Saarland University, Homburg, Germany.
Saarland University · DEHelmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: This study aimed to investigate microglial and macrophage activation in 17 patients who died in the context of a COVID-19 infection in 2020 and 2021. Methods: Through immunohistochemical analysis, the lysosomal marker CD68 was used to detect diffuse parenchymal microglial activity, pronounced perivascular macrophage activation and macrophage clusters. COVID-19 patients were compared to control patients and grouped regarding clinical aspects. Detection of viral proteins was attempted in different regions through multiple commercially available antibodies. Results: Microglial and macrophage activation was most pronounced in the white matter with emphasis in brain stem and cerebellar areas. Analysis of lesion patterns yielded no correlation between disease severity and neuropathological changes. Occurrence of macrophage clusters could not be associated with a severe course of disease or preconditions but represent a more advanced stage of microglial and macrophage activation. Severe neuropathological changes in COVID-19 were comparable to severe Influenza. Hypoxic damage was not a confounder to the described neuropathology. The macrophage/microglia reaction was less pronounced in post COVID-19 patients, but detectable i.e. in the brain stem. Commercially available antibodies for detection of SARS-CoV-2 virus material in immunohistochemistry yielded no specific signal over controls. Conclusion: The presented microglial and macrophage activation might be an explanation for the long COVID syndrome.

Indexed as

CD68CNS infectionCOVID-19immunohistochemistrymacrophageneuropathology

Identifiers

PMID37521293
PMCPMC10374362
OpenAlexW4384156136

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.