Evidence map›Paper›PMID 30451850›Full record

ReviewNPJ schizophrenia2018

Studying and modulating schizophrenia-associated dysfunctions of oligodendrocytes with patient-specific cell systems.

Florian J Raabe, Sabrina Galinski, Sergi Papiol, Peter G Falkai, Andrea Schmitt, Moritz J Rossner

Open access · goldAbstract readReview
In one paragraph

Review in NPJ schizophrenia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Repurposing medications to prevent psychosis.Npj mental health research · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Transcriptional and bioinformatic analysis of GABAFrontiers in molecular neuroscience · 2023
    Article
  12. Article
  13. Activation of AExperimental and therapeutic medicine · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

6 authors at 2 institutions in 2 countries.

Florian J RaabeMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany. florian.raabe@med.uni-muenchen.de.
Sabrina GalinskiMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany.
Sergi PapiolMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany.ORCID http://orcid.org/0000-0001-9366-8728
Peter G FalkaiMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany.
Andrea SchmittMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany.
Moritz J RossnerMolecular and Behavioural Neurobiology, Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany. moritz.rossner@med.uni-muenchen.de.
LMU Klinikum · DEUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postmortem studies in patients with schizophrenia (SCZ) have revealed deficits in myelination, abnormalities in myelin gene expression and altered numbers of oligodendrocytes in the brain. However, gaining mechanistic insight into oligodendrocyte (OL) dysfunction and its contribution to SCZ has been challenging because of technical hurdles. The advent of individual patient-derived human-induced pluripotent stem cells (hiPSCs), combined with the generation of in principle any neuronal and glial cell type, including OLs and oligodendrocyte precursor cells (OPCs), holds great potential for understanding the molecular basis of the aetiopathogenesis of genetically complex psychiatric diseases such as SCZ and could pave the way towards personalized medicine. The development of neuronal and glial co-culture systems now appears to enable the in vitro study of SCZ-relevant neurobiological endophenotypes, including OL dysfunction and myelination, with unprecedented construct validity. Nonetheless, the meaningful stratification of patients before the subsequent functional analyses of patient-derived cell systems still represents an important bottleneck. Here, to improve the predictive power of ex vivo disease modelling we propose using hiPSC technology to focus on representatives of patient subgroups stratified for genomic and/or phenomic features and neurobiological cell systems. Therefore, this review will outline the evidence for the involvement of OPCs/OLs in SCZ in the context of their proposed functions, including myelination and axon support, the implications for hiPSC-based cellular disease modelling and potential strategies for patient selection.

Identifiers

PMID30451850
PMCPMC6242875
OpenAlexW2900972311

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.