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Mutation links bipolar disorder to mitochondrial disease | Tomoaki M. Kato et al

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Abstract rendition of the paper's themes.Mutations in the gene ANT1 may confer a risk for bipolar disorder through a complex interplay between serotonin and mitochondrial signaling in the brain. Credit: Milena Menezes Carvalho/RIKEN National Science InstituteAbstract rendition of the paper's themes.Mutations in the gene ANT1 may confer a risk for bipolar disorder through a complex interplay between serotonin and mitochondrial signaling in the brain. Credit: Milena Menezes Carvalho/RIKEN National Science Institute

June 11, 2018 (MedicalXpress) -- Mutations in the gene ANT1 may confer a risk for bipolar disorder through a complex interplay between serotonin and mitochondrial signaling in the brain.

These two pathways have been separately implicated in bipolar disorder, but the link between levels of the neurotransmitter serotonin and mitochondrial dysfunction had not been established. Researchers at the RIKEN Center for Brain Science (CBS) in Japan now report that mitochondrial dysfunction affects the activity of serotonergic neurons in mice with mutations of ANT1.

Mitochondria are the vital organelles that deliver energy to all cells and mitochondrial damage has been found, for example, in brain imaging of bipolar patients and in post-mortem brains. Roughly 20 percent of patients with mitochondrial disease also have bipolar disorder, a major psychiatric disease characterized by manic and depressive episodes.

Altered serotonin functioning, on the other hand, seems to be involved in bipolar disorder because drugs that target serotonin levels can effectively treat the condition. "Our study suggests that mitochondrial dysfunction can alter activity of serotonergic neurons in bipolar disorder, and this is the first time these two lines of evidence have been linked," says Tadafumi Kato, research group leader at CBS. The research was published on June 8 in the journal Molecular Psychiatry.

(more)

READ MORE: MedicalXpress

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    Monday, June 11 2018
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