Evidence map›Paper›PMID 27138796›Full record

ArticleTranslational psychiatry2016

HPA-axis function and grey matter volume reductions: imaging the diathesis-stress model in individuals at ultra-high risk of psychosis.

I Valli, N A Crossley, F Day, J Stone, S Tognin, V Mondelli, O Howes, L Valmaggia, C Pariante, P McGuire

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Synergistic pathways to psychosis: understanding developmental risk and resilience factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Stress, Environment and Early Psychosis.Current neuropharmacology · 2024
    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

10 authors at 4 institutions in 2 countries.

I ValliDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
N A CrossleyDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
F DayDepartment of Psychology, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
J StoneDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
S TogninDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
V MondelliDepartment of Psychological Medicine, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
O HowesDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
L ValmaggiaDepartment of Psychology, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
C ParianteDepartment of Psychological Medicine, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
P McGuireDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK.
King's College London · GBImperial College London · GBNational Institute for Health Research · GBPontificia Universidad Católica de Chile · CL

Funding

Medical Research Council G0700995Medical Research Council G108/603Medical Research Council MC_U120097115
6 · The paper itself

Abstract

The onset of psychosis is thought to involve interactions between environmental stressors and the brain, with cortisol as a putative mediator. We examined the relationship between the cortisol stress response and brain structure in subjects at ultra-high risk (UHR) for psychosis. Waking salivary cortisol was measured in 22 individuals at UHR for psychosis and 17 healthy controls. Grey matter volume was assessed using magnetic resonance imaging at 3 T. The relationship between the stress response and grey matter volume was investigated using voxel-based analyses. Our predictions of the topography of cortisol action as a structural brain modulator were informed by measures of brain glucocorticoid and mineralcorticoid receptor distribution obtained from the multimodal neuroanatomical and genetic Allen Brain Atlas. Across all subjects, reduced responsivity of the hypothalamus-pituitary-adrenal (HPA) axis was correlated with smaller grey matter volumes in the frontal, parietal and temporal cortex and in the hippocampus. This relationship was particularly marked in the UHR subjects in the right prefrontal, left parahippocampal/fusiform and parietal cortices. The subgroup that subsequently developed psychosis showed a significant blunting of HPA stress response, observed at trend level also in the whole UHR sample. Altered responses to stress in people at high risk of psychosis are related to reductions in grey matter volume in areas implicated in the vulnerability to psychotic disorders. These areas may represent the neural components of a stress vulnerability model.

Indexed as

AdultBrain MappingDisease SusceptibilityFemaleGray MatterHumansHydrocortisoneHypothalamo-Hypophyseal SystemImage Processing, Computer-AssistedMagnetic Resonance ImagingMaleOrgan SizePsychotic DisordersRiskSalivaStress, PsychologicalHydrocortisone

Identifiers

PMID27138796
PMCPMC5070043
OpenAlexW2345556015

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.