Evidence map›Paper›PMID 38510107›Full record

ReviewFrontiers in cellular neuroscience2024

Microglia-neuron interactions in schizophrenia.

Sophia-Marie Hartmann, Johanna Heider, Richard Wüst, Andreas J Fallgatter, Hansjürgen Volkmer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Mismatch negativity matures in adolescence and without sensitivity to microglial depletion.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. UntargetedTranslational psychiatry · 2026
    Article
  13. Article
  14. Review
  15. Review
  16. Microglia as critical mediators linking perinatal immune stress to mental health trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Sophia-Marie Hartmann *Molecular Neurobiology, Department of Pharma and Biotech, NMI Natural and Medical Sciences Institute at the University of Tübingen, Reutlingen, Germany.
Johanna Heider *Molecular Neurobiology, Department of Pharma and Biotech, NMI Natural and Medical Sciences Institute at the University of Tübingen, Reutlingen, Germany.
Richard Wüst *Department of Psychiatry, Tübingen Center for Mental Health (TüCMH), University of Tübingen, Tübingen, Germany.
Andreas J FallgatterDepartment of Psychiatry, Tübingen Center for Mental Health (TüCMH), University of Tübingen, Tübingen, Germany.
Hansjürgen VolkmerMolecular Neurobiology, Department of Pharma and Biotech, NMI Natural and Medical Sciences Institute at the University of Tübingen, Reutlingen, Germany.
University of Tübingen · DENatural and Medical Sciences Institute · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple lines of evidence implicate increased neuroinflammation mediated by glial cells to play a key role in neurodevelopmental disorders such as schizophrenia. Microglia, which are the primary innate immune cells of the brain, are crucial for the refinement of the synaptic circuitry during early brain development by synaptic pruning and the regulation of synaptic plasticity during adulthood. Schizophrenia risk factors as genetics or environmental influences may further be linked to increased activation of microglia, an increase of pro-inflammatory cytokine levels and activation of the inflammasome resulting in an overall elevated neuroinflammatory state in patients. Synaptic loss, one of the central pathological hallmarks of schizophrenia, is believed to be due to excess removal of synapses by activated microglia, primarily affecting glutamatergic neurons. Therefore, it is crucial to investigate microglia-neuron interactions, which has been done by multiple studies focusing on post-mortem brain tissues, brain imaging, animal models and patient iPSC-derived 2D culture systems. In this review, we summarize the major findings in patients and

Indexed as

co-culturecomplement systeminflammationmicroglianeuronschizophreniasynaptic pruning

Identifiers

PMID38510107
PMCPMC10950997
OpenAlexW4392515025

What OpenQuestion holds

Textmetadata
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.