Review of the Literature on Major Mental Disorders in Adult Patients With Mitochondrial Diseases
ABSTRACT Mitochondria are intracellular organelles crucial to the production cellular energy. Mitochondrial disease results from a malfunction in this biochemical cascade. These disorders can affect any organ system, producing diverse signs and symptoms, including psychiatric ones. Several authors argue that mitochondrial dysfunction is related to the pathophysiology of bipolar disorder and schizophrenia. Also, the authors retrieved 19 case reports that describe patients with mitochondrial diseases and psychiatric disorders. Most of these patients have psychiatric presentations that preceded the diagnosis of mitochondrial disease. The most common physical findings are fatigue, muscle weakness with or without atrophy, and hearing loss.
SourceAvailable from: Suleyman Akarsu01/2014; 6(3):1. DOI:10.5455/cap.20140121114707
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ABSTRACT: Transcriptome sequencing of brain samples provides detailed enrichment analysis of differential expression and genetic interactions for evaluation of mitochondrial and coagulation function of schizophrenia. It is implicated that schizophrenia genetic and protein interactions may give rise to biological dysfunction of energy metabolism and hemostasis. These findings may explain the biological mechanisms responsible for negative and withdraw symptoms of schizophrenia and antipsychotic-induced venous thromboembolism. Published BA22 RNA-Seq brain data of 9 schizophrenic patients and 9 controls samples were analyzed. The differentially expressed genes in the BA22 brain samples of schizophrenia are proposed as schizophrenia candidate marker genes (SCZCGs). The genetic interactions between mitochondrial genes and many under-expressed SCZCGs indicate the genetic predisposition of mitochondria dysfunction in schizophrenia. The biological functions of SCZCGs, as listed in the Pathway Interaction Database (PID), indicate that these genes have roles in DNA binding transcription factor, signal and cancer-related pathways, coagulation and cell cycle regulation and differentiation pathways. It is implicated that the energy metabolism and hemostatic process have important roles in the pathogenesis for schizophrenia. The cross-talk of genetic interaction by these co-expressed genes and reached candidate genes may address the key network in disease pathology. The accuracy of candidate genes evaluated from different quantification tools could be improved by crosstalk analysis of overlapping genes in genetic networks.BMC Genomics 12/2014; 15(Suppl 9):S6. DOI:10.1186/1471-2164-15-S9-S6 · 4.04 Impact Factor
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ABSTRACT: 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.