Evidence map›Paper›PMID 39966401›Full record

ArticleSchizophrenia (Heidelberg, Germany)2025

miRNA profiling of hiPSC-derived neurons from monozygotic twins discordant for schizophrenia.

Noora Räsänen, Jari Tiihonen, Marja Koskuvi, Kalevi Trontti, Lesley Cheng, Andrew F Hill, Šárka Lehtonen, Olli Vaurio, Ilkka Ojansuu, Markku Lähteenvuo and 2 more

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In one paragraph

Article in Schizophrenia (Heidelberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Noora RäsänenNeuroscience Center, University of Helsinki, Helsinki, Finland.
Jari TiihonenNeuroscience Center, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0002-0400-6798
Marja KoskuviNeuroscience Center, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0002-1646-9992
Kalevi TronttiNeuroscience Center, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0002-3797-8163
Lesley ChengDepartment of Biochemistry and Chemistry, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Victoria, Australia.
Andrew F HillInstitute for Health and Sport, Victoria University, Melbourne, Australia.
Šárka LehtonenNeuroscience Center, University of Helsinki, Helsinki, Finland.
Olli VaurioDepartment of Forensic Psychiatry, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland.
Ilkka OjansuuDepartment of Forensic Psychiatry, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland.
Markku LähteenvuoDepartment of Forensic Psychiatry, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland.
Olli PietiläinenNeuroscience Center, University of Helsinki, Helsinki, Finland.
Jari KoistinahoHelsinki Institute of Life Science, University of Helsinki, Helsinki, Finland. jari.koistinaho@helsinki.fi.

Funding

Sigrid Juséliuksen Säätiö (Sigrid Jusélius Foundation) N/A
6 · The paper itself

Abstract

Schizophrenia is a complex developmental disorder whose molecular mechanisms are not fully understood. The developmental course of schizophrenia can be modeled with human induced pluripotent stem cell (hiPSC) -derived brain cells that carry patient-specific genetic risk factors for the disorder. Although transcriptomic characterization of the patient-derived cells is a standard procedure, microRNA (miRNA) profiling is less frequently performed. To investigate the role of miRNAs in transcriptomic regulation in schizophrenia, we performed miRNA sequencing for hiPSC-derived neurons from five monozygotic twin pairs discordant for schizophrenia and six controls (CTR). We compared the miRNA expression to differentially expressed genes (DEGs) reported for the same cells in our earlier work. We found 21 DEmiRNAs between the affected twins (AT) and CTR with implications for the regulation of neuronal function. In addition, a separate analysis of three AT with treatment-resistant schizophrenia (TRS), their unaffected twins (UT), and CTR revealed an upregulation of four miRNAs in the UT compared to both AT and CTR. The DEmiRNAs found between the UT and CTR were associated with increased cAMP/PKA signaling and synaptogenesis signaling in the UT. We hypothesize that the upregulation of these processes in the UT could be linked to compensatory features against schizophrenia.

Identifiers

PMID39966401
PMCPMC11836399

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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 OpenQuestion graph.