| Project/Area Number |
23659459
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
KIRA Jun-ichi 九州大学, 医学研究院, 教授 (40183305)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSHITA Takuya 九州大学, 医学研究院, 学術研究員 (00533001)
YOSHIMURA Satoshi 九州大学, 医学研究院, 共同研究員 (20596390)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | コネキシン / 多発性硬化症 / 視神経脊髄炎 / Balo 病 / Balo病 / アクアポリン４ / グリア間相互作用 / アストロサイトパチー |
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| Research Abstract |
To investigate the relationship between astrocytopathy and demyelination, we examined the expression of connexins (Cx). We pathologically evaluated the expressions of astrocytic Cx43/Cx30 and oligodendroglial Cx47/Cx32 among autopsied cases with demyelinating disorders. In Balo’ s disease (BD), Cx43, Cx32 and Cx47 were extensively diminished. In the leading edge of Balo’s lesions, Cx43 and AQP4 loss preceded Cx47 loss. Three cases with multiple sclerosis (MS) and six with neuromyelitis optica (NMO) showed preferential Cx43 and AQP4 loss far beyond the demyelinated areas, while vasculocentric deposition of immunoglobulins or complements was observed in four of the six NMO cases. Some NMO cases showed preferential myelin-associated glycoprotein (MAG) loss in AQP4- and Cx43-diminished active lesions. Our findings indicate that disruption of Cx gap junction and preferential MAG loss could occur in MS, BD and NMO, and could be a common denominator. Inhibition of Cx hemichannels is a possible therapeutic target for demyelinating disorders
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