ReviewBiological psychiatry2018
Mitochondrial Etiology of Neuropsychiatric Disorders.
Review in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 5 of them syntheses 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
104 citing papers in PubMed, 5 syntheses or guidelines pooled it, 178 citations in OpenAlex.
- Translational interdisciplinary research on human chorionic gonadotropin's enhancement of neuroendocrine crosstalk: a novel medical hypothesis for systemic adjunctive treatment of psychiatric disorders.Frontiers in psychiatry · 2025Pooled it
- Comprehensive summary of mitochondrial DNA alterations in the postmortem human brain: A systematic review.EBioMedicine · 2022Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Pooled it
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- Energy-dependent modulation of nucleus accumbens output via K-ATP channel activity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Brain mitochondria as key drivers of cognition and behaviour.Nature reviews. Neuroscience · 2026Review
- Human-Derived Cellular Models in Psychiatry: A Focus on the Olfactory Neuroepithelium.Brain sciences · 2026Review
- First case of schizophrenia and OCD in TK2-related mitochondrial DNA depletion myopathy: a case report.BMC psychiatry · 2026Article
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- Article
- Anxiety-Associated Behaviors Following Ablation ofeNeuro · 2026Article
- Intergenerational neuroimaging's present and future: Considering sex as a biological variable to enhance knowledge of brain development through parent-offspring similarity.Developmental cognitive neuroscience · 2025Review
- Elevated Acetylation of MFN2 is Accompanied by the Disruption of Mitochondrial Energy Metabolism and Inflammation in a Mouse Model of Depression.Molecular neurobiology · 2025Article
- Article
- Biomimetic ferritin nanocages for synergistic co-delivery of metformin and rapamycin restore neurodevelopmental homeostasis in autism spectrum disorders.Journal of nanobiotechnology · 2025Article
- Gene transcription, neurotransmitter, and neurocognition signatures of brain structural-functional coupling variability.Nature communications · 2025Article
- Withania somnifera Regulates Mitochondrial Biogenesis and Energetics in Rat Cortical Neurons: Role of BDNF and SIRT1.Molecular neurobiology · 2025Article
- The Anatomical and Evolutionary Impact of Pain, Pleasure, Motivation, and Cognition: Integrating Energy Metabolism and the Mind-Body BERN (Behavior, Exercise, Relaxation, and Nutrition) Framework.International journal of molecular sciences · 2025Review
- High urea promotes mitochondrial fission and functional impairments in astrocytes inducing anxiety-like behavior in chronic kidney disease mice.Metabolic brain disease · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The brain has the highest mitochondrial energy demand of any organ. Therefore, subtle changes in mitochondrial energy production will preferentially affect the brain. Considerable biochemical evidence has accumulated revealing mitochondrial defects associated with neuropsychiatric diseases. Moreover, the mitochondrial genome encompasses over a thousand nuclear DNA genes plus hundreds to thousands of copies of the maternally inherited mitochondrial DNA (mtDNA). Therefore, partial defects in either the nuclear DNA or mtDNA genes or combinations of the two can be sufficient to cause neuropsychiatric disorders. Inherited and acquired mtDNA mutations have recently been associated with autism spectrum disorder, which parallels previous evidence of mtDNA variation in other neurological diseases. Therefore, mitochondrial dysfunction may be central to the etiology of a wide spectrum of neurological diseases. The mitochondria and the nucleus communicate to coordinate energy production and utilization, providing the potential for therapeutics by manipulating nuclear regulation of mitochondrial gene expression.
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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.