Mitochondrial Dysfunction and Bipolar Disorder

2010 ◽  
pp. 187-200 ◽  
Author(s):  
Tadafumi Kato
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction

scholarly journals Neurobiological basis of bipolar disorder: Mitochondrial dysfunction hypothesis and beyond

2017 ◽  
Vol 187 ◽  
pp. 62-66 ◽  
Author(s):  
Tadafumi Kato
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction

Mitochondrial dysfunction in bipolar disorder

2000 ◽  
Vol 2 (3) ◽  
pp. 180-190 ◽  
Author(s):  
Tadafumi Kato ◽  
Nobumasa Kato
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction

scholarly journals The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors

2021 ◽  
Vol 12 ◽  
Author(s):  
Suzanne Gonzalez
Keyword(s):  
Bipolar Disorder ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Brain Function ◽  
Electron Flow ◽  
Mitochondrial Genes ◽  
Environmental Stressors ◽  
Atp Production ◽  
Co Morbidity

It has been postulated that mitochondrial dysfunction has a significant role in the underlying pathophysiology of bipolar disorder (BD). Mitochondrial functioning plays an important role in regulating synaptic transmission, brain function, and cognition. Neuronal activity is energy dependent and neurons are particularly sensitive to changes in bioenergetic fluctuations, suggesting that mitochondria regulate fundamental aspects of brain function. Vigorous evidence supports the role of mitochondrial dysfunction in the etiology of BD, including dysregulated oxidative phosphorylation, general decrease of energy, altered brain bioenergetics, co-morbidity with mitochondrial disorders, and association with genetic variants in mitochondrial DNA (mtDNA) or nuclear-encoded mitochondrial genes. Despite these advances, the underlying etiology of mitochondrial dysfunction in BD is unclear. A plausible evolutionary explanation is that mitochondrial-nuclear (mitonuclear) incompatibility leads to a desynchronization of machinery required for efficient electron transport and cellular energy production. Approximately 1,200 genes, encoded from both nuclear and mitochondrial genomes, are essential for mitochondrial function. Studies suggest that mitochondrial and nuclear genomes co-evolve, and the coordinated expression of these interacting gene products are essential for optimal organism function. Incompatibilities between mtDNA and nuclear-encoded mitochondrial genes results in inefficiency in electron flow down the respiratory chain, differential oxidative phosphorylation efficiency, increased release of free radicals, altered intracellular Ca2+ signaling, and reduction of catalytic sites and ATP production. This review explores the role of mitonuclear incompatibility in BD susceptibility and resilience against environmental stressors.

Genetic and Biochemical Evidence for Mitochondrial Dysfunction in a Family With Mitochondrial Disease, Bipolar Disorder and Diabetes

2021 ◽  
Vol 89 (9) ◽  
pp. S4-S5
Author(s):  
Angela Duong ◽  
Vanessa Gonçalves ◽  
Ana Andreazza
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Disease ◽  
Biochemical Evidence

Mitochondrial Dysfunction and Oxidative Stress in Bipolar Disorder

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
A. Andreazza
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Bipolar Disorder ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunction ◽  
Frontal Cortex ◽  
Meta Analysis ◽  
Therapeutic Interventions ◽  
Atp Production ◽  
And Oxidative Stress

While we continue to refine our understanding of the pathophysiology of bipolar disorder (BD), several hypotheses have been postulated including a role for monoamines, gamma-amino butyric acid, glutamate, and second messenger signaling pathways. Recently, mitochondrial dysfunction and oxidative stress have been identified by a number of studies, as an important etiological factor in this disorder. Mitochondria play a crucial role in ATP production through oxidative phosphorylation, a process carried out by the electron transport chain (ETC) complexes. During the transfer of electrons along this ETC, the ROS can be generated, especially in complex I and III4. Growing body of evidence suggests the association of mitochondrial dysfunction and BD. Recent DNA microarray analysis in post-mortem frontal cortex and hippocampus revealed that the expression of several mRNAs coding for ETC complexes I-V subunits was decreased in subjects with BD. Supporting the key involvement of oxidative damage in BD, assays conducted with peripheral blood samples have demonstrated that BD is associated with alterations in antioxidant enzymes and increased lipid peroxidation. Recently we found that oxidative damage to lipid is present in the frontal cortex of BD subjects. A meta-analysis suggested that the levels of lipid peroxidation are elevated in BD providing support for oxidative stress hypothesis of BD. Furthermore, BD subjects showed increased DNA damage, as well as, upregulation of apoptotic genes. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

scholarly journals Mitochondrial dysfunction and pathology in bipolar disorder and schizophrenia

2010 ◽  
Vol 29 (3) ◽  
pp. 311-324 ◽  
Author(s):  
Hayley B. Clay ◽  
Stephanie Sillivan ◽  
Christine Konradi
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction

Targeting Mitochondrial Dysfunction for Bipolar Disorder

2020 ◽  
pp. 61-99
Author(s):  
Maya Kuperberg ◽  
Sophie L. A. Greenebaum ◽  
Andrew A. Nierenberg
Keyword(s):  
Bipolar Disorder ◽  
Mitochondrial Dysfunction
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