Evidence map›Paper›PMID 19277608›Full record

ReviewPsychopharmacology2009

Prenatal exposure to infection: a primary mechanism for abnormal dopaminergic development in schizophrenia.

Urs Meyer, Joram Feldon

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Psychopharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Alteration of adaptive behaviors of progeny after maternal mobile phone exposure.Environmental science and pollution research international · 2018
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. The role of inflammation in schizophrenia.Frontiers in neuroscience · 2015
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Evidence for a dysregulated immune system in the etiology of psychiatric disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    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

2 authors at 1 institution in 1 country.

Urs MeyerLaboratory of Behavioral Neurobiology, ETH Zurich, Schorenstrasse 16, Schwerzenbach, Switzerland. urmeyer@ethz.ch
Joram Feldon
ETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationalePrenatal exposure to infection is a notable environmental risk factor in the development of schizophrenia. One prevalent hypothesis suggests that infection-induced disruption of early prenatal brain development predisposes the organism to long-lasting structural and functional brain abnormalities. Many of the prenatal infection-induced functional brain abnormalities appear to be closely associated with imbalances in the mesocorticolimbic dopamine system in adult life, suggesting that disruption of functional and structural dopaminergic development may be at the core of the developmental neuropathology associated with psychosis-related abnormalities induced by prenatal exposure to infection.

objectivesIn this review, we integrate recent findings derived from experimental models in animals with parallel research in humans which supports this hypothesis. We thereby highlight the developmental perspective of abnormal DA functions following in-utero exposure to infection in relation to the developmental and maturational mechanisms potentially involved in schizophrenia.

resultsExperimental investigations show that early prenatal immune challenge can lead to the emergence of early structural and functional alterations in the mesocorticolimbic DA system, long before the onset of the full spectrum of psychosis-associated behavioral and cognitive abnormalities in adulthood.

conclusionsDopaminergic mal-development in general, and following prenatal immune activation in particular, may represent a primary etiopathological mechanism in the development of schizophrenia and related disorders. This hypothesis differs from the view that dopaminergic abnormalities in schizophrenia may be secondary to abnormalities in other brain structures and/or neurotransmitter systems. The existence of primary dopaminergic mechanisms may have important implications for the identification and early treatment of individuals prodromally symptomatic for schizophrenia.

Indexed as

AdultAnimalsDisease Models, AnimalDopamineFemaleHumansLimbic SystemPregnancyPregnancy Complications, InfectiousPrenatal Exposure Delayed EffectsRisk FactorsSchizophreniaDopamine

Identifiers

PMID19277608
OpenAlexW1993826962

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.