| Project/Area Number |
20790865
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
FUKE Satoshi The Institute of Physical and Chemical Research, 精神疾患動態研究チーム, 研究員 (20422660)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | mitochondria / bipolar disorder / mitochondrial polymerase γ / mitochondrial DNA (mtDNA) / mtDNA deletion / ageing / behavioral activity rhythm / brain / bipolar disorde / mitochondrial DNA / aging / accummulation mtDNA deletion / POLG / neuron / mood disorder / BrdU / CPEO |
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| Research Abstract |
We found that exponential accumulation of mtDNAs deletions with ageing, but not mtDNA copy number per cell, are enhanced in muscles and the brains of heterozygous knock-in mice carrying a mutation (D257A) in mtDNA polymerase (PolgA), one of the causative genes of CPEO and related diseases, which often accompany mood disorder. Tissue-specific accumulation of mtDNA deletions suggests that PolgA^<+/D257A> mice are suitable for an animal model of CPEO. PolgA^<+/D257A> mice did not show behavioural changes by conventional behavioural test battery, but showed distorted day-night rhythm. This phenotype resembled the phenotype seen in the other line of mutant mice. There is possibility that accumulation of mtDNA deletions causes mood disorders.
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