Evidence map›Paper›PMID 41620579›Full record

ReviewMolecular psychiatry2026

Neuroinflammation: an unfortunate term to describe schizophrenia.

Vicent Llorca-Bofí, Eduard Parellada, Constanza Morén, Carl M Sellgren, Miquel Bioque

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
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

5 authors.

Vicent Llorca-BofíBarcelona Clínic Schizophrenia Unit (BCSU), Neuroscience Institute, Hospital Clínic of Barcelona; Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM); Department of Medicine, University of Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0001-8467-1335
Eduard ParelladaBarcelona Clínic Schizophrenia Unit (BCSU), Neuroscience Institute, Hospital Clínic of Barcelona; Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM); Department of Medicine, University of Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0003-1131-4980
Constanza MorénBasic and Translational Research Laboratory of Schizophrenia, Barcelona Clínic Schizophrenia Unit (BCSU), Hospital Clínic of Barcelona; Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Basic and Clinical Nursing Department, Nursing Faculty, University of Barcelona, Barcelona, Spain.
Carl M SellgrenDepartment of Physiology and Pharmacology, Karolinska Institutet; Center for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9103-2785
Miquel BioqueBarcelona Clínic Schizophrenia Unit (BCSU), Neuroscience Institute, Hospital Clínic of Barcelona; Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM); Department of Medicine, University of Barcelona, Barcelona, Spain. mbioque@clinic.cat.ORCID http://orcid.org/0000-0001-6887-7149

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia, a chronic psychiatric disorder, has prompted extensive research into its immunological aspects. Studies in genetics, epidemiology, and treatment have revealed immune changes associated with schizophrenia, including shifts in cytokine levels and microglial reactivity within the central nervous system (CNS). However, the term "neuroinflammation" has been used to describe these findings despite inconsistent classical markers, potentially oversimplifying the complex role of immune mediators in neurodevelopment and brain homeostasis. In this paper, we critically examine the limitations of applying "neuroinflammation" to describe immune changes in schizophrenia, focusing on its four classical hallmarks: elevated cytokines, microglial reactivity, peripheral immune cell infiltration, and neurodegeneration. While some alterations in these markers are reported, many findings fall within clinical norms or likely contribute to neurodevelopment, suggesting that the term "neuroinflammation" may misrepresent their role. Instead, we propose using alternative terminology that reflects the broader spectrum of CNS immune responses, both inflammatory and non-inflammatory, and invite the scientific community to join this dialogue to refine terminology. By reframing immune alterations in schizophrenia, we aim to promote accuracy and consistency across medical disciplines, ensuring terminology that accurately represents the underlying biology. This, in turn, will improve communication among researchers and clinicians.

Indexed as

Neuroinflammatory DiseasesSchizophreniaAnimalsBrainCentral Nervous SystemCytokinesHumansInflammationMicrogliaNeurodevelopmentCytokines

Identifiers

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.