Aim. This article reviews several independent lines of evidence that suggest an involvement of mitochondrial dysfunction in the pathogenesis, course and treatment of schizophrenia.
Review. Some studies indicate a dysfunction of the oxidative phosphorylation system and altered mitochondrial-related gene expression. In addition, the interaction between mitochondrial respiration and dopamine, a predominant etiological factor in positive symptoms of schizophrenia, is considered as a possible mechanism underlying the hyper- and hypoactivity cycling in schizophrenia. Antipsychotic drugs inhibit the activity of complex I which is probably implicated in the onset of post-neuroleptic extrapyramidal symptoms.
Conclusions. Understanding the role of mitochondria in schizophrenia may encourage novel treatment approaches, the identification of candidate genes, and new insights into the pathophysiology and etiology of the disorder.