2016 Fiscal Year Final Research Report
Extensive disruption of energy transports via glial syncytium in demyelinating diseases
| Project/Area Number |
26461295
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 多発性硬化症 / 視神経脊髄炎 / グリアシンシチウム / 栄養供給障害 |
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| Outline of Final Research Achievements |
Neuropathological analysis of connexins in MS, NMO, Balo disease was completed. In the spinal cord of NMO, isolated perivascular lesion was frequently found in white matter. We also found that humoral factors derived from Th1 cells decreased the expression of Cx43. We found that the expressions of Cx47 and Cx32 were markedly diminished in oligodendrocytes of spinal gray matter in mutant SOD1-Tg mice.
We investigated the expression pattaren of glucose lactate transporters in demyelinating disorders and found the decreased expression of astrocyte MCT4 in active demyelinating lesions. GLUT1 and MCT1 expressed on the vascular endothelium are retained, and our findings indicated that nutrient supply impairment via glial cells is present in demyelinating diseases.
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| Free Research Field |
脱髄性疾患
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