Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017;16(2):176-186.
doi: 10.2174/1871527315666161213110518.

Mitochondrial Dysfunctions in Bipolar Disorder: Effect of the Disease and Pharmacotherapy

Affiliations
Review

Mitochondrial Dysfunctions in Bipolar Disorder: Effect of the Disease and Pharmacotherapy

Tereza Cikankova et al. CNS Neurol Disord Drug Targets. 2017.

Abstract

Exact pathophysiological mechanisms of bipolar disorder have not been sufficiently clarified. We review the evidence of mitochondrial dysfunctions on the relation between both disease and pharmacotherapy. Mitochondria produce the most of energy-rich molecules of adenosine triphosphate (ATP), apart from energy production they are involved in other functions: regulation of free radicals, antioxidant defenses, lipid peroxidation, calcium metabolism and participate in the intrinsic pathway of apoptosis. According to increasing evidence dysfunctions of mitochondria are associated with affective disorders, a hypothesis of impaired mitochondrial functions has been proposed in bipolar disorder pathogenesis. Mitochondrial DNA mutations and/or polymorphisms, impaired phospholipid metabolism and glycolytic shift, decrease in ATP production, increased oxidative stress and changes of intracellular calcium are concerned in mood disorders and effects of mood stabilizers. Recent studies have also provided data about the positive effects of chronic treatment by mood stabilizers on mitochondrial functions.

Keywords: Bioenergetics; bipolar disorder; electron transport chain complexes; mitochondria; mitochondrial DNA; mood stabilizers; oxidative phosphorylation.

PubMed Disclaimer

Similar articles

Cited by

MeSH terms

Substances

LinkOut - more resources