Bipolar disorder as a mitochondrial disorder
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Introduction
Bipolar disorder (BD) is a chronic psychiatric condition characterized by extreme mood swings, including manic and depressive episodes. Emerging research suggests that mitochondrial dysfunction may play a significant role in the pathophysiology of BD. This synthesis aims to consolidate findings from multiple studies to provide a cohesive understanding of the relationship between mitochondrial dysfunction and bipolar disorder.
Key Insights
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Impaired Energy Metabolism and Mitochondrial Dysfunction:
- Decreased mitochondrial respiration, high-energy phosphates, and pH levels in the brain are observed in BD patients .
- Abnormal brain energy metabolism, including decreased intracellular pH and phosphocreatine levels, has been detected .
- Increased levels of lactate in the brain and cerebrospinal fluid, indicating mitochondrial dysfunction, have been reported.
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Genetic and Molecular Evidence:
- Increased mitochondrial DNA (mtDNA) deletions and polymorphisms are associated with BD .
- Specific mtDNA polymorphisms, such as 5178C and 10398A, are identified as risk factors for BD .
- Downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration is noted .
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Mitochondrial Morphology and Function:
- Abnormal mitochondrial morphology, including smaller mitochondrial areas and altered distribution in brain and peripheral cells, is observed in BD patients .
- Differences in mtDNA copy numbers between BD1 and BD2 patients suggest varying mitochondrial function across BD subtypes.
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Maternal Inheritance and Comorbidity with Mitochondrial Diseases:
- Possible maternal inheritance patterns and comorbidity with mitochondrial diseases, such as mitochondrial diabetes mellitus, are noted .
- Increased levels of the 4977-bp deletion in mtDNA in autopsied brains of BD patients support the mitochondrial dysfunction hypothesis .
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Therapeutic Implications:
- Mood stabilizers may exert their effects through mitochondrial pathways, suggesting mitochondria as potential therapeutic targets .
- Animal models with mtDNA deletions exhibit BD-like phenotypes, providing a basis for developing new treatments .
Conclusion
The collective evidence strongly supports the hypothesis that mitochondrial dysfunction is a significant component of bipolar disorder. Impaired energy metabolism, genetic mutations, and abnormal mitochondrial morphology are consistently observed in BD patients. These findings highlight the potential of targeting mitochondrial pathways for therapeutic interventions and underscore the need for further research to elucidate the specific mechanisms by which mitochondrial dysfunction contributes to the symptoms of bipolar disorder.
Sources and full results
Most relevant research papers on this topic
Mitochondrial Dysfunction as the Molecular Basis of Bipolar Disorder
Mitochondrial dysfunction in bipolar disorder: Evidence, pathophysiology and translational implications
Mitochondrial dysfunction in bipolar disorder.
Abnormalities in mitochondrial structure in cells from patients with bipolar disorder.
Differences in mitochondrial DNA copy number between patients with bipolar I and II disorders.
Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis.
Neurobiological basis of bipolar disorder: Mitochondrial dysfunction hypothesis and beyond
Is bipolar disorder a mitochondrial disease?
Mitochondrial DNA polymorphisms in bipolar disorder.
A model of the mitochondrial basis of bipolar disorder
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