ReviewMolecular neuropsychiatry2015
Evidence of Mitochondrial Dysfunction within the Complex Genetic Etiology of Schizophrenia.
Review in Molecular neuropsychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers, 1 of them a synthesis that pooled 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.
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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- A Comprehensive Analysis of Nuclear-Encoded Mitochondrial Genes in Schizophrenia.Biological psychiatry · 2018Pooled it
- The Role of Cytochrome P450 Holoenzyme Metabolism in the Origin of Neuropathologies.International journal of molecular sciences · 2026Review
- Circulating Cell-Free DNA in Psychiatric Disorders: Current Evidence, Inflammation-Based Stratification, and Future Perspectives.International journal of molecular sciences · 2026Review
- A new mechanism underlying mitochondrial dysfunction in schizophrenia - attenuated mRNA transport of the complex I subunit NDUFV2 by its pseudogene NDUFV2P1.Schizophrenia (Heidelberg, Germany) · 2026Article
- From brain bioenergetics to hypothalamic glucoregulation: A shared-systems hypothesis for intrinsic dysglycemia in schizophrenia.Reviews in endocrine & metabolic disorders · 2026Review
- Maternal Immune Activation Leads to Mitochondrial Dysfunction and a Social Deficit in Offspring That Is Reversed by Nicotinamide Riboside.Nutrients · 2026Article
- Investigating neural impairments in psychotic disorders using electroencephalography and cortical spheroids.Translational psychiatry · 2026Article
- Altered Co-Expression Patterns of Mitochondrial NADH-Dehydrogenase Genes in the Prefrontal Cortex of Rodent ADHD Models.International journal of molecular sciences · 2025Article
- Cerebrolysin ameliorates ketamine-mediated anxiety and cognitive impairments via modulation of mitochondrial function and CREB/PGC-1α pathway.Molecular brain · 2025Article
- Repurposing medications to prevent psychosis.Npj mental health research · 2025Review
- Molecular overlaps of neurological manifestations of COVID-19 and schizophrenia from a proteomic perspective.European archives of psychiatry and clinical neuroscience · 2025Article
- High frequency of mitochondrial DNA rearrangements in the peripheral blood of adults with intellectual disability.Journal of intellectual disability research : JIDR · 2025Article
- Neuronal Synaptic Communication and Mitochondrial Energetics in Human Health and Disease.Advances in experimental medicine and biology · 2025Review
- Mitochondrial dysfunction in psychiatric disorders.Schizophrenia research · 2024Review
- Cognitive improvements linked to lysophosphatidylethanolamine after olanzapine treatment in drug-naïve first-episode schizophrenia.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Direct targets of MEF2C are enriched for genes associated with schizophrenia and cognitive function and are involved in neuron development and mitochondrial function.PLoS genetics · 2024Article
- Elevations in the Mitochondrial Matrix Protein Cyclophilin D Correlate With Reduced Parvalbumin Expression in the Prefrontal Cortex of Patients With Schizophrenia.Schizophrenia bulletin · 2024Article
- Effects of antipsychotic drugs on energy metabolism.European archives of psychiatry and clinical neuroscience · 2024Article
- The Underlying Neurobiological Mechanisms of Psychosis: Focus on Neurotransmission Dysregulation, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2024Review
- Analysis of human neuronal cells carrying ASTN2 deletion associated with psychiatric disorders.Translational psychiatry · 2024Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedErratum.2016
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Genetic evidence has supported the hypothesis that schizophrenia (SZ) is a polygenic disorder caused by the disruption in function of several or many genes. The most common and reproducible cellular phenotype associated with SZ is a reduction in dendritic spines within the neocortex, suggesting alterations in dendritic architecture may cause aberrant cortical circuitry and SZ symptoms. Here, we review evidence supporting a multifactorial model of mitochondrial dysfunction in SZ etiology and discuss how these multiple paths to mitochondrial dysfunction may contribute to dendritic spine loss and/or underdevelopment in some SZ subjects. The pathophysiological role of mitochondrial dysfunction in SZ is based upon genomic analyses of both the mitochondrial genome and nuclear genes involved in mitochondrial function. Previous studies and preliminary data suggest SZ is associated with specific alleles and haplogroups of the mitochondrial genome, and also correlates with a reduction in mitochondrial copy number and an increase in synonymous and nonsynonymous substitutions of mitochondrial DNA. Mitochondrial dysfunction has also been widely implicated in SZ by genome-wide association, exome sequencing, altered gene expression, proteomics, microscopy analyses, and induced pluripotent stem cell studies. Together, these data support the hypothesis that SZ is a polygenic disorder with an enrichment of mitochondrial targets.
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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.