| Budget Amount *help |
¥141,830,000 (Direct Cost: ¥109,100,000、Indirect Cost: ¥32,730,000)
Fiscal Year 2016: ¥27,170,000 (Direct Cost: ¥20,900,000、Indirect Cost: ¥6,270,000)
Fiscal Year 2015: ¥27,170,000 (Direct Cost: ¥20,900,000、Indirect Cost: ¥6,270,000)
Fiscal Year 2014: ¥27,300,000 (Direct Cost: ¥21,000,000、Indirect Cost: ¥6,300,000)
Fiscal Year 2013: ¥27,040,000 (Direct Cost: ¥20,800,000、Indirect Cost: ¥6,240,000)
Fiscal Year 2012: ¥33,150,000 (Direct Cost: ¥25,500,000、Indirect Cost: ¥7,650,000)
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| Outline of Final Research Achievements |
Because mitochondrial disease frequently accompanies bipolar disorder, we developed a model mouse carrying mutant Polg, a causative gene of mitochondrial diseases. The mice showed recurrent spontaneous episodes satisfying the clinical criteria of major depression that responded to anti-depressive treatments and showed alteration of corticosteroid. We identified that mutant mitochondrial DNA is accumulated in paraventricular thalamic nucleus (PVT). Inhibition of neural transmission of PVT neurons caused similar episodes in mice. Cells with mitochondrial dysfunction were found also in paraventricular region of the postmortem brains of patients with mitochondrial disease and mood symptoms. The present findings are expected to lead to development of new mood stabilizers and diagnostic methods.
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