ReviewMolecular psychiatry2026
Neuroinflammation: an unfortunate term to describe schizophrenia.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Aging in Schizophrenia: Clinical, Biological, and Psychosocial Perspectives.Geriatrics (Basel, Switzerland) · 2026Review
- Association between serum non-enzymatic antioxidants and cognitive impairment in drug-naïve patients with schizophrenia.BMC psychiatry · 2026Article
- Review
- Clinical correlates and cognitive associations of the neutrophil-to-lymphocyte ratio in first-episode psychosis and at-risk mental states.Frontiers in psychiatry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
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
Identifiers
41620579What 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.