| Project/Area Number |
24790889
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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 |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
MASAKI Katsuhisa 九州大学, 医学(系)研究科(研究院), 助教 (90612903)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | コネキシン / 多発性硬化症 / 視神経脊髄炎 / Balo病 / ギャップ結合 / グリアシンシチウム |
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| Research Abstract |
To investigate the relationship between astrocytopathy and demyelination, we examined the expression of connexins (Cx). We evaluated the expressions of astrocytic Cx43/Cx30 and oligodendrocytic Cx47/Cx32 among autopsied cases with demyelinating disorders. In Balo disease (BD), Cx43, Cx32 and Cx47 were extensively diminished. In the leading edge area, 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. 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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