Evidence map›Paper›PMID 26988846›Full record

ReviewPsychopharmacology2016

Is it time for immunopsychiatry in psychotic disorders?

Marion Leboyer, José Oliveira, Ryad Tamouza, Laurent Groc

Abstract readReview
PubMed Publisher
In one paragraph

Review in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Charting the proteome landscape in major psychiatric disorders: From biomarkers to biological pathways towards drug discovery.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2022
    Pooled it
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  8. Exploring causal mechanisms of psychosis risk.Neuroscience and biobehavioral reviews · 2024
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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

4 authors at 4 institutions in 1 country.

Marion LeboyerUniversité Paris-Est, INSERM U955, Laboratoire Psychiatrie Translationnelle, et AP-HP, DHU Pe-PSY, Pole de Psychiatrie et d'addictologie des Hôpitaux Universitaires Henri Mondor, et fondation FondaMental, F-94000, Créteil, France. marion.leboyer@inserm.fr.
José OliveiraUniversité Paris-Est, INSERM U955, Laboratoire Psychiatrie Translationnelle, et AP-HP, DHU Pe-PSY, Pole de Psychiatrie et d'addictologie des Hôpitaux Universitaires Henri Mondor, et fondation FondaMental, F-94000, Créteil, France.
Ryad TamouzaINSERM, U1160, Hôpital Saint Louis, Laboratoire Jean Dausset and LabEx Transplantex, Hôpital Saint Louis, Université Paris Diderot, Sorbonne Paris-Cité, Paris, France.
Laurent GrocUniversité de Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000, Bordeaux, France.
Assistance Publique – Hôpitaux de Paris · FRHôpital Saint-Louis · FRHôpitaux Universitaires Henri-Mondor · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionImmune dysregulation is suggested to play an important aetiological role in schizophrenia (SZ) and bipolar disorder (BD) potentially driving neurodevelopmental pathways. Immune dysfunction may precede the onset of psychiatric disorders and parallel the development of multiaxial comorbidity, including suicidal behaviour and metabolic and autoimmune disorders. Depicting the source of the chronic low-grade inflammatory component in SZ and BD is thus a research priority. Strong environmental insults early in life, such as infections, acting on a background of genetic vulnerability, may induce potent and enduring inflammatory responses setting a state of liability to second-hit environmental encounters, namely childhood trauma, drug abuse or additional infectious exposures. The immunogenetic background of susceptibility, suggested to be not only lying within the HLA locus but also implicating inherited deficits of the innate immune system, may amplify the harmful biological effects of infections/psychosocial stress leading to the manifestation of a broad range of psychiatric symptoms.

objectivesThe present review aims to discuss the following: (i) biological arguments in favour of a chronic low-grade inflammation in SZ and BD and its potential origin in the interaction between the immunogenetic background and environmental infectious insults, and (ii) the consequences of this inflammatory dysfunction by focusing on N-methyl-D-aspartate (NMDA) receptor antibodies and activation of the family of human endogenous retroviruses (HERVs).

conclusionsSpecific therapeutic approaches targeting immune pathways may lead the way to novel personalized medical interventions, improvement of quality of life and average life expectancy of psychiatric patients, if not even prevent mood episodes and psychotic symptoms.

Indexed as

PsychoneuroimmunologyAnimalsHumansImmunotherapyInflammationPsychiatryPsychotic DisordersBipolar disorderGene-environment interactionsHERV-WImmunogeneticsImmunopsychiatryNMDA receptorSchizophrenia

Identifiers

PMID26988846
OpenAlexW2300880694

What OpenQuestion holds

Textmetadata
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.