Mechanism of onset of diabetic normal pressure hydrocephalus by oral microorganism-derived TLR Ligands
| Project/Area Number |
26861584
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
KAJI CHIAKI 福岡歯科大学, 口腔歯学部, 助教 (60707214)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 糖尿病 / 水頭症 / 脳脊髄液脳関門 / P-cadherin / podoplanin / 脳室脈絡叢 / 脈絡叢上皮 / CML / TLR / Porphyromonas gingivalis / 脈絡叢線維芽細胞 / コラーゲン / 免疫 / 感染 |
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| Outline of Final Research Achievements |
In this study, we found that the expression of P-cadherin and podoplanin in the ventricles of diabetic mice is decreased, and that diabetic mice regularly given P-cadherin and podoplanin antibodies intraperitoneally reach the humane endpoint. P-cadherin and podoplanin are molecules that contribute to cell adhesion and cytoskeleton formation in cooperation with N-cadherin and others. It is thought that in the diabetic brain the reduction of P-cadherin and podoplanin may cause the dysfunction of adhesion between the ventricle cells, which is responsible for the hydrocephalus due to the deterioration of brain cerebrospinal fluid barrier function.
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Report
(4 results)
Research Products
(1 results)
