AI Article Synopsis

  • Mitochondria are essential for energy production and calcium signaling in neurons, and dysfunctions in these processes are linked to psychiatric disorders like schizophrenia and bipolar disorder.
  • Research on mitochondria's role in these conditions is limited due to difficulties in studying dynamic changes in function.
  • Recent advancements in stem cell-derived human neuronal models provide promising tools to better understand mitochondrial deficits in psychiatric disorders and highlight the need for integrating these models with animal studies for comprehensive insights.

Article Abstract

Mitochondria play a crucial role in neuronal function, especially in energy production, the generation of reactive oxygen species, and calcium signaling. Multiple lines of evidence have suggested the possible involvement of mitochondrial deficits in major psychiatric disorders, such as schizophrenia and bipolar disorder. This review will outline the current understanding of the physiological role of mitochondria and their dysfunction under pathological conditions, particularly in psychiatric disorders. The current knowledge about mitochondrial deficits in these disorders is somewhat limited because of the lack of effective methods to dissect dynamic changes in functional deficits that are directly associated with psychiatric conditions. Human neuronal cell model systems have been dramatically developed in recent years with the use of stem cell technology, and these systems may be key tools for overcoming this dilemma and improving our understanding of the dynamic changes in the mitochondrial deficits in patients with psychiatric disorders. We introduce recent discoveries from new experimental models and conclude the discussion by referring to future perspectives. We emphasize the significance of combining studies of human neuronal cell models with those of other experimental systems, including animal models.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469392PMC
http://dx.doi.org/10.1016/j.biopsych.2018.01.007DOI Listing

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