Evidence map›Paper›PMID 22488257›Full record

ReviewMolecular psychiatry2012

Neurodevelopmental model of schizophrenia: update 2012.

J L Rapoport, J N Giedd, N Gogtay

Open access · greenAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 373 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
373citing papers in PubMed, 6 pooled it
25.1field-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

373 citing papers in PubMed, 6 syntheses or guidelines pooled it, 778 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Pooled it
  6. Pooled it
  7. Review
  8. Polygenic risk meets early trauma: toward a neuropsychodevelopmental model of schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

313 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

J L RapoportChild Psychiatry Branch, NIH, NIMH, Bethesda, MD 20892, USA. rapoporj@mail.nih.gov
J N Giedd
N Gogtay
National Institutes of Health · US

Funding

Childhood Onset SchizophreniaZIAMH002581 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI RAPOPORT, JUDITH L. · 2009 to 2017
$25.5M
Pediatric Brain ImagingZIAMH002794 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI RAPOPORT, JUDITH L. · 2009 to 2015
$15.3M
Intramural NIH HHS Z99 MH999999
6 · The paper itself

Abstract

The neurodevelopmental model of schizophrenia, which posits that the illness is the end state of abnormal neurodevelopmental processes that started years before the illness onset, is widely accepted, and has long been dominant for childhood-onset neuropsychiatric disorders. This selective review updates our 2005 review of recent studies that have impacted, or have the greatest potential to modify or extend, the neurodevelopmental model of schizophrenia. Longitudinal whole-population studies support a dimensional, rather than categorical, concept of psychosis. New studies suggest that placental pathology could be a key measure in future prenatal high-risk studies. Both common and rare genetic variants have proved surprisingly diagnostically nonspecific, and copy number variants (CNVs) associated with schizophrenia are often also associated with autism, epilepsy and intellectual deficiency. Large post-mortem gene expression studies and prospective developmental multi-modal brain imaging studies are providing critical data for future clinical and high-risk developmental brain studies. Whether there can be greater molecular specificity for phenotypic characterization is a subject of current intense study and debate, as is the possibility of neuronal phenotyping using human pluripotent-inducible stem cells. Biological nonspecificity, such as in timing or nature of early brain development, carries the possibility of new targets for broad preventive treatments.

Indexed as

Models, NeurologicalAge FactorsBrainGenetic Predisposition to DiseaseHumansNeuroimagingPluripotent Stem CellsRisk FactorsSchizophrenia

Identifiers

PMID22488257
PMCPMC3504171
OpenAlexW2004469093

What OpenQuestion holds

Textmetadata
LicenceTDM
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.