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Neural Plasticity
Volume 2015 (2015), Article ID 408136, 10 pages
Review Article

The Potential Role of the NLRP3 Inflammasome as a Link between Mitochondrial Complex I Dysfunction and Inflammation in Bipolar Disorder

1Department of Pharmacology and Toxicology, University of Toronto, 1 King’s College Circle, Toronto, ON, Canada M5S 1A8
2Department of Psychiatry, University of Toronto, 1 King’s College Circle, Toronto, ON, Canada M5S 1A8
3Centre of Addiction and Mental Health, 250 College Street, Toronto, ON, Canada M5T 1R8

Received 6 August 2014; Accepted 6 November 2014

Academic Editor: Rodrigo Machado-Vieira

Copyright © 2015 Helena Kyunghee Kim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondrial dysfunction and activation of the inflammatory system are two of the most consistently reported findings in bipolar disorder (BD). More specifically, altered levels of inflammatory cytokines and decreased levels of mitochondrial complex I subunits have been found in the brain and periphery of patients with BD, which could lead to increased production of mitochondrial reactive oxygen species (ROS). Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3). Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade. In this review, we discuss the potential role of the NLRP3 inflammasome as a link between complex I dysfunction and inflammation in BD and its therapeutic implications.