| Project/Area Number |
16K19999
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 小胞体ストレス応答 / 脳虚血 / 神経細胞死 / 脳血管関門破綻 / 脳神経疾患 |
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| Outline of Final Research Achievements |
Deletion of ATF6α gene, a master transcriptional factor in the unfolded protein response worsened the disruption of blood brain barrier and increased the infarction volume of mice after middle cerebral artery occlusion(MCAO) in the subacute phase.
However, there was no significant difference in the infarction volume between wild-type and ATF6α knockout mice in the chronic phase. We already reported that ATF6α deficiency suppresses microglial activation and inflammation of mice in multiple sclerosis model. Deterioration of microglial activation was also observed in ATF6αKO mice after MCAO, which probably affect the infarct size in chronic phase.
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