ReviewTranslational psychiatry2017
Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization.
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.
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.
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.
Prevalence of Traumatic Events and Post-traumatic Stress Disorder in Immigrant and Non-immigrant Patients With Psychotic Disorder
Who cites it
147 citing papers in PubMed, 11 syntheses or guidelines pooled it, 282 citations in OpenAlex.
- Immune System Alterations in Treatment-Resistant Schizophrenia: A Systematic Review of the Current Evidence and Future Directions.International journal of molecular sciences · 2026Pooled it
- Inflammatory cytokine alterations in genetic and clinical high risk groups of psychosis: a systematic review and network meta-analysis.Psychological medicine · 2026Pooled it
- Adjunctive berberine for schizophrenia with metabolic syndrome: a systematic review and meta-analysis.Frontiers in psychiatry · 2026Pooled it
- Importance of the dysregulation of the kynurenine pathway on cognition in schizophrenia: a systematic review of clinical studies.European archives of psychiatry and clinical neuroscience · 2023Pooled it
- Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review.Molecular neurobiology · 2022Pooled it
- White-matter free-water diffusion MRI in schizophrenia: a systematic review and meta-analysis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Pooled it
- Pooled it
- A Meta-analysis of Immune Parameters, Variability, and Assessment of Modal Distribution in Psychosis and Test of the Immune Subgroup Hypothesis.Schizophrenia bulletin · 2019Pooled it
- Synaptic loss in schizophrenia: a meta-analysis and systematic review of synaptic protein and mRNA measures.Molecular psychiatry · 2019Pooled it
- Positron Emission Tomography Studies of the Glial Cell Marker Translocator Protein in Patients With Psychosis: A Meta-analysis Using Individual Participant Data.Biological psychiatry · 2018Pooled it
- Kinetics of Cytokine Levels during Antipsychotic Treatment in Schizophrenia: A Meta-Analysis.The international journal of neuropsychopharmacology · 2018Pooled it
- Exercise Intervention in Individuals at Clinical High Risk for Psychosis: Benefits to Fitness, Symptoms, Hippocampal Volumes, and Functional Connectivity.Schizophrenia bulletin · 2022Trial
- Association between TLR2 polymorphisms (- 196-174 Ins/Del, R677W, R753Q, and P631H) and schizophrenia in a Tunisian population.Immunologic research · 2021Trial
- Protective Effects of Gallic Acid on Oxidative and Inflammatory Markers in the Hippocampus and Prefrontal Cortex of a Ketamine-Induced Schizophrenia-like Model.Brain sciences · 2026Article
- Article
- Psychosis in the Context of Travel, Substance Use, and Media Exposure: A Stress-Diathesis Perspective.Cureus · 2026Article
- High-density lipoprotein (HDL) in older patients with schizophrenia: implications for clinical and cognitive outcomes.BMC psychiatry · 2026Article
- Peripheral inflammation mediates cognitive deficits in drug-naive schizophrenia through hippocampal-thalamo-visual circuitry dysfunction.Schizophrenia (Heidelberg, Germany) · 2026Article
- Gut microbial signatures in schizophrenia: exploring archaea, fungi, and bacteria.BMC psychiatry · 2026Article
- CD163+ perivascular macrophages in schizophrenia: a research framework for testing macrophage-related mechanisms.Frontiers in psychiatry · 2026Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
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.
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What OpenQuestion holds
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.