Evidence map›Paper›PMID 40050441›Full record

ArticleNature neuroscience2025

Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19.

Rebeka Fekete, Alba Simats, Eduárd Bíró, Balázs Pósfai, Csaba Cserép, Anett D Schwarcz, Eszter Szabadits, Zsuzsanna Környei, Krisztina Tóth, Erzsébet Fichó and 14 more

Abstract read
In one paragraph

Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Human brain matters: Navigating the neuropathology of COVID-19.Brain pathology (Zurich, Switzerland) · 2026
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  16. Combination antiviral and anti-inflammatory therapy mitigates persistent neurological deficits in mice post SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

24 authors.

Rebeka FeketeMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Alba SimatsInstitute for Stroke and Dementia Research, LMU University Hospital, LMU Munich, Munich, Germany.
Eduárd BíróLaboratory of Inflammation-Physiology, Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Balázs PósfaiMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Csaba CserépMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Anett D SchwarczMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Eszter SzabaditsMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Zsuzsanna KörnyeiMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Krisztina TóthMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Erzsébet FichóCytocast Hungary Kft, Budapest, Hungary.ORCID http://orcid.org/0000-0002-3965-8438
János SzalmaCytocast Hungary Kft, Budapest, Hungary.
Sára VidaMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Anna KellermayerMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Csaba DávidDepartment of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0003-4221-9468
László AcsádyLendület Laboratory of Thalamus Research, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Levente KontraBioinformatics Unit, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Carlos Silvestre-RoigInstitute for Experimental Pathology (ExPat), Center for Molecular Biology of Inflammation, WWU Muenster, Muenster, Germany.
Judit MoldvayI. Department of Pulmonology, National Korányi Institute of Pulmonology, Budapest, Hungary.
János FillingerDepartment of Pathology, National Korányi Institute of Pulmonology, Budapest, Hungary.
Attila Csikász-NagyCytocast Hungary Kft, Budapest, Hungary.ORCID http://orcid.org/0000-0002-2919-5601
Tibor HortobágyiInstitute of Pathology, Faculty of Medicine, University of Szeged, Szeged, Hungary.ORCID http://orcid.org/0000-0001-5732-7942
Arthur LieszInstitute for Stroke and Dementia Research, LMU University Hospital, LMU Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-9069-2594
Szilvia BenkőLaboratory of Inflammation-Physiology, Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Ádám DénesMomentum Laboratory of Neuroimmunology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary. denes.adam@koki.hun-ren.hu.ORCID http://orcid.org/0000-0001-6919-4905

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 is associated with diverse neurological abnormalities, but the underlying mechanisms are unclear. We hypothesized that microglia, the resident immune cells of the brain, are centrally involved in this process. To study this, we developed an autopsy platform allowing the integration of molecular anatomy, protein and mRNA datasets in postmortem mirror blocks of brain and peripheral organ samples from cases of COVID-19. We observed focal loss of microglial P2Y12R, CX3CR1-CX3CL1 axis deficits and metabolic failure at sites of virus-associated vascular inflammation in severely affected medullary autonomic nuclei and other brain areas. Microglial dysfunction is linked to mitochondrial injury at sites of excessive synapse and myelin phagocytosis and loss of glutamatergic terminals, in line with proteomic changes of synapse assembly, metabolism and neuronal injury. Furthermore, regionally heterogeneous microglial changes are associated with viral load and central and systemic inflammation related to interleukin (IL)-1 or IL-6 via virus-sensing pattern recognition receptors and inflammasomes. Thus, SARS-CoV-2-induced inflammation might lead to a primarily gliovascular failure in the brain, which could be a common contributor to diverse COVID-19-related neuropathologies.

Indexed as

COVID-19InflammationInterleukin-1Interleukin-6MicrogliaAgedBrainFemaleHumansMaleMiddle AgedPandemicsSARS-CoV-2IL6 protein, humanInterleukin-1Interleukin-6

Identifiers

PMID40050441
PMCPMC11893456

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.