Evidence map›Paper›PMID 26666733›Full record

ReviewCurrent neuropharmacology2016

Animal Models of Maternal Immune Activation in Depression Research.

Marianne Ronovsky, Stefanie Berger, Barbara Molz, Angelika Berger, Daniela D Pollak

Abstract readReview
In one paragraph

Review in Current neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Multiple Complement Pathway-related Proteins Might Regulate Immunopathogenesis of Major Depressive Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Inflammation as a Mechanism of Bipolar Disorder Neuroprogression.Current topics in behavioral neurosciences · 2021
    Article
  15. Article
  16. COVID-19 in pregnancy: Placental and neonatal involvement.American journal of reproductive immunology (New York, N.Y. : 1989) · 2020
    Article
  17. Article
  18. The fetal origins of mental illness.American journal of obstetrics and gynecology · 2019
    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

5 authors.

Marianne Ronovsky
Stefanie Berger
Barbara Molz
Angelika Berger
Daniela D PollakDepartment of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, A-1090 Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDepression and schizophrenia are debilitating mental illnesses with significant socio-economic impact. The high degree of comorbidity between the two disorders, and shared symptoms and risk factors, suggest partly common pathogenic mechanisms. Supported by human and animal studies, maternal immune activation (MIA) has been intimately associated with the development of schizophrenia. However, the link between MIA and depression has remained less clear, in part due to the lack of appropriate animal models.

objectiveHere we aim to summarize findings obtained from studies using MIA animal models and discuss their relevance for preclinical depression research.

methodsResults on molecular, cellular and behavioral phenotypes in MIA animal models were collected by literature search (PubMed) and evaluated for their significance for depression.

resultsSeveral reports on offspring depression-related behavioral alterations indicate an involvement of MIA in the development of depression later in life. Depression-related behavioral phenotypes were frequently paralleled by neurogenic and neurotrophic deficits and modulated by several genetic and environmental factors.

conclusionLiterature evidence analyzed in this review supports a relevance of MIA as animal model for a specific early life adversity, which may prime an individual for the development of distinct psychopathologies later life. MIA animal models may present a unique tool for the identification of additional exogenous and endogenous factors, which are required for the manifestation of a specific neuropsychiatric disorder, such as depression, later in life. Hereby, novel insights into the molecular mechanisms involved in the pathophysiology of depression may be obtained, supporting the identification of alternative therapeutic strategies.

Indexed as

AnimalsBrainDisease Models, AnimalFemalePregnancyPregnancy Complications, InfectiousPrenatal Exposure Delayed EffectsSchizophrenia

Identifiers

PMID26666733
PMCPMC5050397

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Registered trials

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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.