ReviewMolecular psychiatry2025
Glial cell deficits are a key feature of schizophrenia: implications for neuronal circuit maintenance and histological differentiation from classical neurodegeneration.
Review in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Efficacy and safety of Nrf2 activators for schizophrenia: a systematic review and meta-analysis.European archives of psychiatry and clinical neuroscience · 2026Pooled it
- Multimodal microglial and kynurenine pathway alterations across the affective-psychosis spectrum: a systematic review of patterns, heterogeneity, and dimensional implications.Molecular psychiatry · 2026Pooled it
- Early life experiences, the neural epigenome and affective disorder risk.Nature reviews. Neuroscience · 2026Review
- Astrocyte-Derived Extracellular Vesicles and the Evolution of Neural Complexity: Perspectives on Vesicle-Mediated Neuron-Glia Communication.Molecular neurobiology · 2026Review
- Adolescent Exposure to a THC-Rich Cannabis Extract Produces Genotype-Dependent Effects on Cognition and Glial Morphology in Serine Racemase Mutant Mice.Journal of neurochemistry · 2026Article
- Neuronal genetic risk within the multicellular landscape of schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Review
- Neuroglia Alterations in the Olfactory Bulbs in Patients with Schizophrenia: An Exploratory Postmortem Study.Life (Basel, Switzerland) · 2026Article
- Myo-inositol concentration in the medial prefrontal cortex is associated with changes in brain white matter microstructure in early psychosis.Translational psychiatry · 2026Article
- Cellular Diversity Underpins Cortical Organization and Disease Vulnerability in the Human Brain.Neuroscience bulletin · 2026Article
- NfL and GFAP quantification and associations with mental health in recreational cannabis users-Results from the Swiss study on recreational cannabis access via pharmacies.Molecular neurobiology · 2026Article
- Glucocorticoids and cell fate in the developing brain: Neuroendocrine mechanisms shaping developmental trajectories.Journal of neuroendocrinology · 2026Review
- Regulatory Genomic Circuitry of Brain Age by Integrative Functional Genomic Analyses.Genomics, proteomics & bioinformatics · 2025Article
- Decreased levels of platelet-derived growth factor subtypes and superoxide dismutase isoenzymes in early-onset schizophrenia.Schizophrenia (Heidelberg, Germany) · 2025Article
- Age-Dependent Redistribution of the Life-Important Enzyme in the Retina: Adult Müller Glial Cells' Endfeet Lack Spermine Synthase Expression.Biomolecules · 2025Article
- Combining phenomics with transcriptomics reveals cell-type-specific morphological and molecular signatures of the 22q11.2 deletion.Nature communications · 2025Article
- Therapeutic Targeting of the α7 Nicotinic Receptor: Challenges and Prospects for Cognitive Improvement in Alzheimer's and Schizophrenia.Basic & clinical pharmacology & toxicology · 2025Review
- A single dose of haloperidol decanoate induces short-term hippocampal neuroinflammation: focus on the glial response.Pharmacological reports : PR · 2025Article
- Human endogenous retrovirus W family envelope protein (ERVWE1) regulates macroautophagy activation and micromitophagy inhibition via NOXA1 in schizophrenia.Virologica Sinica · 2025Article
- Influence of antipsychotic drugs on microglia-mediated neuroinflammation in schizophrenia: perspectives in an astrocyte-microglia co-culture model.Frontiers in psychiatry · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunctional glial cells play a pre-eminent role in schizophrenia pathophysiology. Post-mortem studies have provided evidence for significantly decreased glial cell numbers in different brain regions of individuals with schizophrenia. Reduced glial cell numbers are most pronounced in oligodendroglia, but reduced astrocyte cell densities have also been reported. This review highlights that oligo- and astroglial deficits are a key histopathological feature in schizophrenia, distinct from typical changes seen in neurodegenerative disorders. Significant deficits of oligodendrocytes in schizophrenia may arise in two ways: (i) demise of mature functionally compromised oligodendrocytes; and (ii) lack of mature oligodendrocytes due to failed maturation of progenitor cells. We also analyse in detail the controversy regarding deficits of astrocytes. Regardless of their origin, glial cell deficits have several pathophysiological consequences. Among these, myelination deficits due to a reduced number of oligodendrocytes may be the most important factor, resulting in the disconnectivity between neurons and different brain regions observed in schizophrenia. When glial cells die, it appears to be through degeneration, a process which is basically reversible. Thus, therapeutic interventions that (i) help rescue glial cells (ii) or improve their maturation might be a viable option. Since antipsychotic treatment alone does not seem to prevent glial cell loss or maturation deficits, there is intense search for new therapeutic options. Current proposals range from the application of antidepressants and other chemical agents as well as physical exercise to engrafting healthy glial cells into brains of schizophrenia patients.
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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 Socratic graph.