Mitochondrial dysfunction as a critical event in the pathophysiology of bipolar disorder.

Abstract

The understanding of the pathophysiology of bipolar disorder (BD) remains modest, despite recent advances in neurobiological research. The mitochondrial dysfunction hypothesis of bipolar disorder has been corroborated by several studies involving postmortem brain analysis, neuroimaging, and specific biomarkers in both rodent models and humans. Evidence suggests that BD might be related to abnormal mitochondrial morphology and dynamics, neuroimmune dysfunction, and atypical mitochondrial metabolism and oxidative stress pathways. Mitochondrial dysfunction in mood disorders is also associated with abnormal Ca2+ levels, glutamate excitotoxicity, an imbalance between pro- and antiapoptotic proteins towards apoptosis, abnormal gene expression of electron transport chain complexes, and decreased ATP synthesis. This paper aims to review and discuss the implications of mitochondrial dysfunction in BD etiology and to explore mitochondria as a potential target for novel therapeutic agents.

• Authors: Giselli Scaini, Taylor Andrews, Camila N C Lima, Deborah Benevenuto, Emilio L Streck, João Quevedo
• Journal: Mitochondrion (Mitochondrion) Vol. 57 Pg. 23-36 (03 2021) ISSN: 1872-8278 [Electronic] Netherlands
• PMID: 33340709 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2020 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

Chemical References

• Glutamic Acid
• Calcium

Topics

• Apoptosis
• Bipolar Disorder (metabolism, pathology)
• Brain (metabolism)
• Calcium (metabolism)
• Gene Expression Regulation
• Glutamic Acid (metabolism)
• Humans
• Mitochondria (metabolism)
• Oxidative Stress