Evidence map›Paper›PMID 25496904›Full record

ReviewNeuroscience and biobehavioral reviews2015

Fetal programming of schizophrenia: select mechanisms.

Monojit Debnath, Ganesan Venkatasubramanian, Michael Berk

Abstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
13.2field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  9. The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Copy Number Variations and Schizophrenia.Molecular neurobiology · 2023
    Review
  15. Extracellular Vesicles in Mental Disorders: A State-of-art Review.International journal of biological sciences · 2023
    Review
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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

3 authors at 2 institutions in 2 countries.

Monojit DebnathDepartment of Human Genetics, National Institute of Mental Health & Neurosciences, Bangalore 560029, India. Electronic address: monozeet@gmail.com.
Ganesan VenkatasubramanianTranslational Psychiatry Laboratory, Neurobiology Research Centre and Department of Psychiatry, National Institute of Mental Health & Neurosciences, Hosur Road, Bangalore 560029, India.
Michael BerkIMPACT Strategic Research Centre, School of Medicine, Deakin University, Barwon Health, Geelong, Victoria, Australia; Department of Psychiatry, The Florey Institute of Neuroscience and Mental Health, and Orygen, The National Centre of Excellence in Youth Mental Health, University of Melbourne, Parkville, Australia.
National Institute of Mental Health and Neurosciences · INBarwon Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence indicates that schizophrenia is associated with adverse intrauterine experiences. An adverse or suboptimal fetal environment can cause irreversible changes in brain that can subsequently exert long-lasting effects through resetting a diverse array of biological systems including endocrine, immune and nervous. It is evident from animal and imaging studies that subtle variations in the intrauterine environment can cause recognizable differences in brain structure and cognitive functions in the offspring. A wide variety of environmental factors may play a role in precipitating the emergent developmental dysregulation and the consequent evolution of psychiatric traits in early adulthood by inducing inflammatory, oxidative and nitrosative stress (IO&NS) pathways, mitochondrial dysfunction, apoptosis, and epigenetic dysregulation. However, the precise mechanisms behind such relationships and the specificity of the risk factors for schizophrenia remain exploratory. Considering the paucity of knowledge on fetal programming of schizophrenia, it is timely to consolidate the recent advances in the field and put forward an integrated overview of the mechanisms associated with fetal origin of schizophrenia.

Indexed as

AnimalsFetal DevelopmentHumansSchizophreniaDietEpigeneticsFetal programmingInfectionInflammationNeurodevelopmentOxidative stressPerinatalPrenatalSchizophreniaStress

Identifiers

PMID25496904
PMCPMC7112550
OpenAlexW1980729314

What OpenQuestion holds

Textmetadata
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.