Mitochondrial Dysfunction, Altered Mitochondrial Oxygen, and Energy Metabolism Associated with the Pathogenesis of Schizophrenia

Iveta Fizíková, Jozef Dragašek, Peter Račay, Iveta Fizíková, Jozef Dragašek, Peter Račay

Abstract

The significant complexity of the brain can lead to the development of serious neuropsychiatric disorders, including schizophrenia. A number of mechanisms are involved in the etiopathogenesis of schizophrenia, pointing to its complexity and opening a new perspective on studying this disorder. In this review of currently published studies, we focused on the contribution of mitochondria to the process, with an emphasis on oxidative damage, ROS, and energy metabolism. In addition, we point out the influence of redox imbalance, which can lead to the occurrence of oxidative stress with increased lipid peroxidation, linked to the formation of toxic aldehydes such as 4-hydroxynonenal (4-HNE) and HNE protein adducts. We also analysed the role of lactate in the process of energy metabolism and cognitive functions in schizophrenia.

Keywords: energy metabolism; mitochondria; oxidative stress; schizophrenia.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Representative Western blot detection of HNE conjugates of plasma proteins of control volunteers (C) and schizophrenia patients (P). Positions of molecular mass standards are indicated. Adapted from [21].
Figure 2
Figure 2
Overview of mechanisms of mitochondrial dysfunction leading to neuroprogressive changes in schizophrenia. LDH—lactate dehydrogenase, OXPHOS—oxidative phosphorylation, ROS—reactive oxygen species, I–IV—enzyme complexes of OXPHOS.

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