Mitochondrial pathways in bipolar disorder: Mechanisms and implications

Abstract Mitochondria represent a convergence point for survival and death signals triggered by both intracellular and extracellular cues and play a crucial role in brain function and cognition. Several lines of evidence have proposed the possible involvement of the mitochondrial dysfunction on the neurobiology of bipolar disorder (BD). Converging evidence suggests that mitochondrial dysfunction may include decreases in mitochondrial respiration, high-energy phosphates and pH, changes in mitochondrial morphology, increases in mitochondrial DNA polymorphisms, and downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration. Moreover the impaired mitochondrial function might lead to a disruption of normal neural plasticity, contribute to the atrophic changes, and ultimately promote the neurocognitive deficits and progression of BD. Therefore this chapter highlights the latest findings that support the theory of mitochondrial dysfunction in BD, providing an overview of the physiological and genetic components of mitochondria and pieces of evidence for mitochondrial abnormalities in BD.