Evidence map›Paper›PMID 36256663›Full record

ArticlePloS one2022

The interleukin-6/interleukin-23/T helper 17-axis as a driver of neuro-immune toxicity in the major neurocognitive psychosis or deficit schizophrenia: A precision nomothetic psychiatry analysis.

Hussein Kadhem Al-Hakeim, Ali Fattah Al-Musawi, Abbas Al-Mulla, Arafat Hussein Al-Dujaili, Monojit Debnath, Michael Maes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  7. Zinc in psychosis (Review).Molecular medicine reports · 2025
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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

6 authors at 5 institutions in 5 countries.

Hussein Kadhem Al-HakeimDepartment of Chemistry, College of Science, University of Kufa, Kufa, Iraq.ORCID 0000-0001-6143-5196
Ali Fattah Al-MusawiDepartment of Clinical Pharmacy and Laboratory Sciences, College of Pharmacy, University of Al-Kafeel, Kufa, Iraq.
Abbas Al-MullaMedical Laboratory Technology Department, College of Medical Technology, The Islamic University, Najaf, Iraq.
Arafat Hussein Al-DujailiSenior Clinical Psychiatrist at the Faculty of Medicine, University of Kufa, Kufa, Iraq.
Monojit DebnathDepartment of Human Genetics, National Institute of Mental Health and Neurosciences, Bangalore, India.
Michael MaesDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
University of Kufa · IQDeakin University · AUIraqi University · IQNational Institute of Mental Health and Neurosciences · INUniversity of Alkafeel · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSchizophrenia and especially deficit schizophrenia (DSCZ) are characterized by increased activity of neuroimmunotoxic pathways and a generalized cognitive decline (G-CoDe). There is no data on whether the interleukin (IL)-6/IL-23/T helper 17 (IL-6/IL-23/Th17)-axis is more associated with DSCZ than with non-deficit schizophrenia (NDSCZ) and whether changes in this axis are associated with the G-CoDe and the phenome (a factor extracted from all symptom domains) of schizophrenia.

methodsThis study included 45 DSCZ and 45 NDSCZ patients and 40 controls and delineated whether the IL-6/IL-23/Th17 axis, trace elements (copper, zinc) and ions (magnesium, calcium) are associated with DSCZ, the G-CoDe and the schizophrenia phenome.

resultsIncreased plasma IL-23 and IL-6 levels were associated with Th17 upregulation, assessed as a latent vector (LV) extracted from IL-17, IL-21, IL-22, and TNF-α. The IL-6/IL-23/Th17-axis score, as assessed by an LV extracted from IL-23, IL-6, and the Th17 LV, was significantly higher in DSCZ than in NDSCZ and controls. We discovered that 70.7% of the variance in the phenome was explained by the IL-6/IL-23/Th17-axis (positively) and the G-CoDe and IL-10 (both inversely); and that 54.6% of the variance in the G-CoDe was explained by the IL-6/IL-23/Th17 scores (inversely) and magnesium, copper, calcium, and zinc (all positively).

conclusionThe pathogenic IL-6/IL-23/Th17-axis contributes to the generalized neurocognitive deficit and the phenome of schizophrenia, especially that of DSCZ, due to its key role in peripheral inflammation and neuroinflammation and its consequent immunotoxic effects on neuronal circuits. These clinical impairments are more prominent in subjects with lowered IL-10, magnesium, calcium, and zinc.

Indexed as

PsychiatryPsychotic DisordersSchizophreniaTrace ElementsCalciumCopperHumansInterleukin-10Interleukin-17Interleukin-23Interleukin-6InterleukinsMagnesiumTh17 CellsTumor Necrosis Factor-alphaZincCalciumCopperInterleukin-10Interleukin-17Interleukin-23Interleukin-6InterleukinsMagnesiumTrace ElementsTumor Necrosis Factor-alphaZinc

Identifiers

PMID36256663
PMCPMC9578624
OpenAlexW4306711183

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Registered trials

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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.