Evidence map›Paper›PMID 28170004›Full record

ReviewTranslational psychiatry2017

Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization.

O D Howes, R McCutcheon

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04867447 (Prevalence of Traumatic Events and Post-traumatic Stress Disorder in Immigrant and Non-immigrant Patients With Psychotic Disorder), which is not on this map. Cited by 147 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 11 pooled it
14.0field-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.

NCT04867447 completednot on this mapstarted 2019, after this paper: background citation

Prevalence of Traumatic Events and Post-traumatic Stress Disorder in Immigrant and Non-immigrant Patients With Psychotic Disorder

TypeobservationalSponsorParc de Salut MarRan2019 to 2023Enrolled199ConditionsPsychotic Disorders, Psychological Trauma, Stress, Psychological, Cross-Cultural ComparisonArmsPsychological trauma evaluation
3 · Its place in the literature

Who cites it

147 citing papers in PubMed, 11 syntheses or guidelines pooled it, 282 citations in OpenAlex.

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  6. White-matter free-water diffusion MRI in schizophrenia: a systematic review and meta-analysis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
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87 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

2 authors at 1 institution in 1 country.

O D HowesDepartment of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
R McCutcheonDepartment of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.ORCID 0000-0003-1102-2566
King's College London · GB

Funding

Medical Research Council G0700995Medical Research Council MC_U120097115Medical Research Council MR/N026063/1Wellcome Trust
6 · The paper itself

Abstract

An interaction between external stressors and intrinsic vulnerability is one of the longest standing pathoaetiological explanations for schizophrenia. However, novel lines of evidence from genetics, preclinical studies, epidemiology and imaging have shed new light on the mechanisms that may underlie this, implicating microglia as a key potential mediator. Microglia are the primary immune cells of the central nervous system. They have a central role in the inflammatory response, and are also involved in synaptic pruning and neuronal remodeling. In addition to immune and traumatic stimuli, microglial activation occurs in response to psychosocial stress. Activation of microglia perinatally may make them vulnerable to subsequent overactivation by stressors experienced in later life. Recent advances in genetics have shown that variations in the complement system are associated with schizophrenia, and this system has been shown to regulate microglial synaptic pruning. This suggests a mechanism via which genetic and environmental influences may act synergistically and lead to pathological microglial activation. Microglial overactivation may lead to excessive synaptic pruning and loss of cortical gray matter. Microglial mediated damage to stress-sensitive regions such as the prefrontal cortex and hippocampus may lead directly to cognitive and negative symptoms, and account for a number of the structural brain changes associated with the disorder. Loss of cortical control may also lead to disinhibition of subcortical dopamine-thereby leading to positive psychotic symptoms. We review the preclinical and in vivo evidence for this model and consider the implications this has for treatment, and future directions.

Indexed as

Schizophrenic PsychologySocial EnvironmentAnimalsBrainDisease SusceptibilityDopamineGray MatterHippocampusHumansInflammationMicrogliaNeurogliaNeuronal PlasticityPsychological TraumaSchizophreniaStress, PsychologicalDopamine

Identifiers

PMID28170004
PMCPMC5438023
OpenAlexW2587178939

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.