Mitochondria are unique and important organelles in terms of energy production for the eukaryotic cell. Through complexes of the electron transport chain embedded in the mitochondrial membrane, the cell is able produce large amounts of ATP. Mitochondria posses their own genome, some of which encodes for the subunits of these protein complexes. From the comorbidity of psychotic symptoms seen in those with mitochondrial disorders, the change in efficiency of cellular respiration has started to emerge as a target for research for understanding the mechanisms and potential therapeutic approaches in mental disorders. Schizophrenia is the hallmark of psychotic diseases and its diverse symptoms have been implicated to have its primary effects in the mesolimbic and mesocortical pathways in the brain. Mitochondrial concentrations in these areas and mutations within the mitochondrial genome are an active area of research. Additionally, the effects of mood stabilizers and antipsychotics in terms of oxidative phosphorylation have been examined in proteomics, DNA and RNA microarray technology, and neuroimaging to name a few. In this article, we make an attempt to discuss and analyze the effects of mutations in the mitochondrial genome with respect to electron transport chain and cellular respiration in individuals affected with schizophrenia.
Key words: Mitochondria, schizophrenia, electron transport chain, antipsychotics, mood stabilizers.
Copyright © 2021 Author(s) retain the copyright of this article.
This article is published under the terms of the Creative Commons Attribution License 4.0