| Project/Area Number |
15K15071
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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 |
General medical chemistry
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| Research Institution | University of Fukui (2016)
Osaka City University (2015) |
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Principal Investigator |
Yamada Masami 福井大学, 学術研究院医学系部門, 教授 (10322851)
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| Research Collaborator |
MORIYAMA Tetsuji 福井大学, 学術研究院医学系部門・医学領域・生命情報医科学講座・分子生体情報学分野, 助教 (50627990)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 神経細胞遊走障害 / 細胞内物質輸送 / 細胞質ダイニン / 微小管分子モーター / 発達障害 / αーシヌクレイン / 神経細胞遊走（移動）障害 / LIS1 / カルパイン阻害薬 / 創薬スクリーニング / 精神・神経疾患 / 精神発達遅滞 / 微小管関連因子 / 遺伝性神経疾患 |
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| Outline of Final Research Achievements |
In the current study, we searched for a common drug target for genetic diseases that occur in conjunction with neuronal migration disorders, using intracellular transport and molecular dynamics related to microtubule molecule motors as indicators. The current study revealed that microtubule fragments (transportable microtubules: tMT), which are structures that serve as carriers for transport complexes, move along microtubules. These include cytoplasmic dynein, previously identified by our research group, and α-synuclein, which forms Lewy bodies that are characteristic of neurodegenerative disorders, including Parkinson’s disease. In the future, we plan to investigate whether a mutation/deletion of α-synuclein would result in a marked change in the severity of neuronal migration disorders. Furthermore, we plan to conduct comprehensive screening of low molecular weight compounds that would restore or ameliorate decreased neuronal migration activity.
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