ArticleTranslational psychiatry2022
Mitochondria DNA copy number, mitochondria DNA total somatic deletions, Complex I activity, synapse number, and synaptic mitochondria number are altered in schizophrenia and bipolar disorder.
Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.
- Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation.Schizophrenia bulletin · 2025Pooled it
- Whole blood mitochondrial copy number in clinical populations with mood disorders: A meta-analysis: Blood mitochondrial copy number and mood disorders.Psychiatry research · 2024Pooled it
- Enhanced axonal mitochondrial motility and neural activity-induced energy deficits destabilize synaptic transmission in models of bipolar disorder.Nature communications · 2026Article
- Powering the mind: deciphering the shared genetic architecture between mitochondrial DNA copy number and major psychiatric disorders.Molecular psychiatry · 2026Article
- Integrative multi-omics identifiesPsychological medicine · 2026Article
- Article
- Cortical Transcriptomic Profiling Reveals Cellular and Mitochondrial Adaptive Stress Signatures That Differ Between Schizophrenia and Bipolar Disorder.Schizophrenia bulletin · 2026Article
- ERVWE1 Impairs Mitochondrial Homeostasis and Promotes Neuronal Apoptosis via the miR-27b-3p/BNIP3 Axis in Schizophrenia.Viruses · 2026Article
- Integrative Multi-Omics Mendelian Randomization Reveals Oxidative Stress Mechanisms in Major Depressive Disorder, Bipolar Disorder, and Schizophrenia.Antioxidants (Basel, Switzerland) · 2026Article
- Premature aging in serious mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Altered Co-Expression Patterns of Mitochondrial NADH-Dehydrogenase Genes in the Prefrontal Cortex of Rodent ADHD Models.International journal of molecular sciences · 2025Article
- Neuron-Derived Extracellular Vesicles: Emerging Regulators in Central Nervous System Disease Progression.Molecular neurobiology · 2025Review
- Single-molecule DNA analysis implicates brain mitochondria pathology in bipolar disorder.Molecular psychiatry · 2025Article
- Increased Rate of Unique Mitochondrial DNA Deletion Breakpoints in Young Adults With Early-Life Stress.Biological psychiatry global open science · 2025Article
- Exploring genetic associations and drug targets for mitochondrial proteins and schizophrenia risk.Schizophrenia (Heidelberg, Germany) · 2025Article
- Plant-derived polyphenolic compounds for managing schizophrenia: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- Cross-species analysis uncovers the mitochondrial stress response in the hippocampus as a shared mechanism in mouse early life stress and human depression.Neurobiology of stress · 2024Article
- The Potential Role of the Ketogenic Diet in Serious Mental Illness: Current Evidence, Safety, and Practical Advice.Journal of clinical medicine · 2024Review
- Research progress in mitochondrial quality control in schizophrenia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Impaired mitochondrial function in bipolar disorder and alcohol use disorder: a case study usingPsychoradiology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is a neurobiological phenomenon implicated in the pathophysiology of schizophrenia and bipolar disorder that can synergistically affect synaptic neurotransmission. We hypothesized that schizophrenia and bipolar disorder share molecular alterations at the mitochondrial and synaptic levels. Mitochondria DNA (mtDNA) copy number (CN), mtDNA common deletion (CD), mtDNA total deletion, complex I activity, synapse number, and synaptic mitochondria number were studied in the postmortem human dorsolateral prefrontal cortex (DLPFC), superior temporal gyrus (STG), primary visual cortex (V1), and nucleus accumbens (NAc) of controls (CON), and subjects with schizophrenia (SZ), and bipolar disorder (BD). The results showed (i) the mtDNA CN is significantly higher in DLPFC of both SZ and BD, decreased in the STG of BD, and unaltered in V1 and NAc of both SZ and BD; (ii) the mtDNA CD is significantly higher in DLPFC of BD while unaltered in STG, V1, and NAc of both SZ and BD; (iii) The total deletion burden is significantly higher in DLPFC in both SZ and BD while unaltered in STG, V1, and NAc of SZ and BD; (iv) Complex I activity is significantly lower in DLPFC of both SZ and BD, which is driven by the presence of medications, with no alteration in STG, V1, and NAc. In addition, complex I protein concentration, by ELISA, was decreased across three cortical regions of SZ and BD subjects; (v) The number of synapses is decreased in DLPFC of both SZ and BD, while the synaptic mitochondria number was significantly lower in female SZ and female BD compared to female controls. Overall, these findings will pave the way to understand better the pathophysiology of schizophrenia and bipolar disorder for therapeutic interventions.
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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.