SynthesisFrontiers in cell and developmental biology2026
Bioenergetic impairment in schizophrenia: role of mitochondrial signaling in synaptic dysfunction - a systematic review.
Synthesis in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Untargeted metabolomics reveals plasma metabolic dysregulation in schizophrenia.BMC psychiatry · 2026Article
- Peripheral neurotransmitter metabolic signatures in schizophrenia: a targeted metabolomics study.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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Mitochondrial dysfunction represents a critical pathophysiological mechanism in schizophrenia, potentially linking bioenergetic impairment to synaptic dysfunction and cognitive deficits. Converging evidence suggests that deficits in oxidative phosphorylation may drive the synaptic pathology contributing to treatment-resistant cognitive and negative symptoms. Objective: To systematically review the evidence linking mitochondrial bioenergetic dysfunction to synaptic impairment in schizophrenia, examining structural, functional, and molecular mechanisms across multiple methodological approaches. Methods: Following PRISMA guidelines, we searched PubMed/MEDLINE, Embase, PsycINFO, and Web of Science from 2000 to 2025 for original research studies investigating mitochondrial function and synaptic dysfunction in schizophrenia. Two independent reviewers screened 2,224 articles, with 29 studies meeting inclusion criteria. Quality was assessed using the Newcastle-Ottawa Scale (median score 7/9). Results: Twenty-nine studies representing 2,847 participants demonstrated consistent mitochondrial dysfunction across Conclusion: Mitochondrial bioenergetic impairment represents a core, potentially modifiable pathophysiological mechanism driving synaptic dysfunction in schizophrenia. Regional specificity (prefrontal cortex, hippocampus) and cell-type selectivity (pyramidal neurons) provide mechanistic insights into cognitive symptom profiles. Early presence and progressive worsening suggest critical intervention windows. Mitochondrial-targeted therapies merit investigation as novel approaches for treatment-resistant cognitive and negative symptoms.
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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.