| Project/Area Number |
22790834
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経変性疾患 / 筋萎縮性側索硬化症 / マイクログリア / 貪食 / 筋委縮性側索硬化症 / ミクログリア |
|---|
| Research Abstract |
First, we evaluatebyimmunohistochemistry the microglialbehaviorinspinalcord lesion of ALS mouse model. We found microglia uptaked, or surrounded the SOD1 aggregates in the spinal cord of the SOD1G85R transgenic mouse at symptomatic stage. Therefore wehy pothes ized that these microglia reflected the state of"frustrated phagocytosis"when microglia could not digest SOD1 aggregates fully. Next, in order to quantify th uptake of aggregates into microglia, we establishedthe system tomeasure the fluorescent beads incorporated into the phagocytes Using the system, we compared the SOD1G85R expressing-microglia with wild-type ones, but no difference was found. We confirmedtheaggregates ofthe SOD1WTor G85Rfibrilswere incorpotrated into microglia when they were added into medium. Then we made the mutant SOD1 aggregate-mimics by adsorb SOD1G85Rinto beads andexamined the ability ofwild-type orSOD1G85R-expressing microglia t incorporate them, butno difference was found.
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