2006 Fiscal Year Final Research Report Summary
Mechanism of neuroprotection by the heat shock proteins in amyotrophic lateral sclerosis model mice (SOD1-G93S transgenic mice)
| Project/Area Number |
17590872
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Kyoto University |
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Principal Investigator |
KAWAMATA Jun Kyoto university, Graduate school of medicine, Assistant Professor, 医学研究科, 助手 (60360814)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMOHARA Shun Sapporo medical university, Faculty of medicine, Professor, 医学部, 教授 (60235687)
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| Project Period (FY) |
2005 – 2006
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| Keywords | ALS / HSP / SOD1 / Neuroprotection |
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| Research Abstract |
1.Establishing proteome map of nervous system of ALS transgenic mice (Gurney et al. Science 1994)
We have made proteome map (soluble fraction and insoluble fraction) of nervous system of young and old ALS Tg mice.
2.Analysis of therapeutic effect and proteome change by administering neuroprotective HSP inducers to the ALS transgenic mice
We have administrated several possible neuroprotective drugs and analyzed proteomic change and life period, so far we could not document significant therapeutic effect of HSP inducers on ALS Tg mice
3.Searching for SOD1 binding proteins using culture cells
We searched for possible SOD1 binding protein candidates by immunoprecipitation using Neuro2A cell line. Two HSPs, HSc70 and HSP105, are found to be SOD1 binding proteins. Our finding was published on Journal of Neurochemistry.
4.Possible therapeutic method based on our hypothesis
We found that HSP105 suppresses the formation of mutant SOD1 containing aggregates in cultured cell. This result suggests that techniques that raise levels of HSP105 might be promising tools for alleviation of the mutant SOD1 toxicity.
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