Evidence map›Paper›PMID 23298853›Full record

ReviewNeuroscience2013

Stress and neurodevelopmental processes in the emergence of psychosis.

C W Holtzman, H D Trotman, S M Goulding, A T Ryan, A N Macdonald, D I Shapiro, J L Brasfield, E F Walker

Abstract readReview
In one paragraph

Review in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
13.8field-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

110 citing papers in PubMed, 240 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Synergistic pathways to psychosis: understanding developmental risk and resilience factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Stress, Environment and Early Psychosis.Current neuropharmacology · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

50 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

8 authors at 1 institution in 1 country.

C W HoltzmanDepartment of Psychology, Emory University, 36 Eagle Row, Atlanta, GA 30322, United States.
H D Trotman
S M Goulding
A T Ryan
A N Macdonald
D I Shapiro
J L Brasfield
E F Walker
Emory University · US

Funding

Research Training for Prevention of Suicide and Pyschosis: A Public Health ModelT32MH082745 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI BECK, AARON T · 2010 to 2014
$1.2M
NIMH NIH HHS L30 MH095165NIMH NIH HHS T32 MH082745
6 · The paper itself

Abstract

The notion that stress plays a role in the etiology of psychotic disorders, especially schizophrenia, is longstanding. However, it is only in recent years that the potential neural mechanisms mediating this effect have come into sharper focus. The introduction of more sophisticated models of the interplay between psychosocial factors and brain function has expanded our opportunities for conceptualizing more detailed psychobiological models of stress in psychosis. Further, scientific advances in our understanding of adolescent brain development have shed light on a pivotal question that has challenged researchers; namely, why the first episode of psychosis typically occurs in late adolescence/young adulthood. In this paper, we begin by reviewing the evidence supporting associations between psychosocial stress and psychosis in diagnosed patients as well as individuals at clinical high risk for psychosis. We then discuss biological stress systems and examine changes that precede and follow psychosis onset. Next, research findings on structural and functional brain characteristics associated with psychosis are presented; these findings suggest that normal adolescent neuromaturational processes may go awry, thereby setting the stage for the emergence of psychotic syndromes. Finally, a model of neural mechanisms underlying the pathogenesis of psychosis is presented and directions for future research strategies are explored.

Indexed as

AdolescentAdolescent DevelopmentAnimalsBrainHumansHypothalamo-Hypophyseal SystemPituitary-Adrenal SystemPsychotic DisordersStress, PsychologicalACTHadrenocorticotrophic hormoneassociative striatumASTBDNFbrain-derived neurotrophic factorbrain developmentcatechol-O-methyltransferaseCHRclinical high riskclinical high-riskCOMTcorticotrophin-releasing hormoneCRHDADEXdexamethasonedexamethasone suppression testdopamineDSTESMExperience Sampling Methodgenetic high riskGHRglucocorticoid receptorsGRshomovanillic acidHPAHVAhypothalamic–pituitary–adrenalhypothalamic–pituitary–adrenal (HPA) axisMetmethioninemethylenetetrahydrofolate reductasemineralocorticoid receptorsmonozygoticMRsMTHFRMZNAPLSneuregulin 1NMDAN-methyl-d-aspartateNorth American Prodrome Longitudinal StudyNR1odds ratioORPCPphencyclidinePOMCprodromepro-opiomelanocortinpsychosisSAMsensorimotor striatumSIPSSMSTstressStructured Interview for Prodromal Syndromessympathetic–adrenal–medullaryValvaline

Identifiers

PMID23298853
PMCPMC4140178
OpenAlexW2001750328

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.