ReviewMolecular psychiatry2016
Molecular substrates of schizophrenia: homeostatic signaling to connectivity.
Review in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Brain structural abnormalities in treatment-resistant schizophrenia.Molecular psychiatry · 2026Pooled it
- Oxidative Stress and Inflammation in First-Episode Psychosis: A Systematic Review and Meta-analysis.Schizophrenia bulletin · 2019Pooled it
- Analysis of differential gene expression mediated by clozapine in human postmortem brains.Schizophrenia research · 2017Pooled it
- N-acetylcysteine in a Double-Blind Randomized Placebo-Controlled Trial: Toward Biomarker-Guided Treatment in Early Psychosis.Schizophrenia bulletin · 2018Trial
- The Pathobiological Underpinnings of Psychosis: From the Stress-Related Hypothesis to a Multisystemic Approach.NeuroSci · 2025Review
- Uridine Phosphorylase 1 as a Biomarker Associated with Glycolysis in Acute Lung Injury.Inflammation · 2025Article
- Rutin ameliorates imiquimod-induced psoriasis-like skin lesions by inhibiting oxidative stress injury and the inflammatory response in mice via the Keap1/Nrf2 signaling pathway.Scientific reports · 2025Article
- Increased Complement C4 in a Sparse Neuronal Subset Induces Network-Wide Transcriptomic Alterations in the Prefrontal Cortex.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial Oxidative Phosphorylation System Dysfunction in Schizophrenia.International journal of molecular sciences · 2025Review
- The Role of Neuroglia in the Development and Progression of Schizophrenia.Biomolecules · 2024Review
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- Illuminating the dark kinome: utilizing multiplex peptide activity arrays to functionally annotate understudied kinases.Cell communication and signaling : CCS · 2024Article
- Nuclear GAPDH in cortical microglia mediates cellular stress-induced cognitive inflexibility.Molecular psychiatry · 2024Article
- Biomarkers for Psychosis: Are We There Yet? Umbrella Review of 1478 Biomarkers.Schizophrenia bulletin open · 2024Article
- Multiple genes in a single GWAS risk locus synergistically mediate aberrant synaptic development and function in human neurons.Cell genomics · 2023Article
- Longitudinal changes in brain metabolites in healthy controls and patients with first episode psychosis: a 7-Tesla MRS study.Molecular psychiatry · 2023Article
- Neurodevelopmental trajectories, polygenic risk, and lipometabolism in vulnerability and resilience to schizophrenia.BMC psychiatry · 2023Article
- The adenosine hypothesis of schizophrenia into its third decade: From neurochemical imbalance to early life etiological risks.Frontiers in cellular neuroscience · 2023Review
- Article
- Aggregative trans-eQTL analysis detects trait-specific target gene sets in whole blood.Nature communications · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Schizophrenia (SZ) is a devastating psychiatric condition affecting numerous brain systems. Recent studies have identified genetic factors that confer an increased risk of SZ and participate in the disease etiopathogenesis. In parallel to such bottom-up approaches, other studies have extensively reported biological changes in patients by brain imaging, neurochemical and pharmacological approaches. This review highlights the molecular substrates identified through studies with SZ patients, namely those using top-down approaches, while also referring to the fruitful outcomes of recent genetic studies. We have subclassified the molecular substrates by system, focusing on elements of neurotransmission, targets in white matter-associated connectivity, immune/inflammatory and oxidative stress-related substrates, and molecules in endocrine and metabolic cascades. We further touch on cross-talk among these systems and comment on the utility of animal models in charting the developmental progression and interaction of these substrates. Based on this comprehensive information, we propose a framework for SZ research based on the hypothesis of an imbalance in homeostatic signaling from immune/inflammatory, oxidative stress, endocrine and metabolic cascades that, at least in part, underlies deficits in neural connectivity relevant to SZ. Thus, this review aims to provide information that is translationally useful and complementary to pathogenic hypotheses that have emerged from genetic studies. Based on such advances in SZ research, it is highly expected that we will discover biomarkers that may help in the early intervention, diagnosis or treatment of SZ.
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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.