| Project/Area Number |
17019006
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TSUJI Shoji The University of Tokyo, 医学部附属病院, 教授 (70150612)
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| Co-Investigator(Kenkyū-buntansha) |
ONODERA Osamu 新潟大学, 大学院・医学系研究科, 准教授 (20303167)
MURAYAMA Shigeo 東京都高齢者研究福祉振興財団, 東京都老人総合研究所臨床科学研究グループ, 参事研究員 (50183653)
後藤 順 東京大学, 医学部附属病院, 講師 (10211252)
高橋 祐二 東京大学, 医学部附属病院, 助教 (00372392)
百瀬 義雄 (百瀬 義男) 東京大学, 医学部附属病院, 特任助教 (30359624)
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| Co-Investigator(Renkei-kenkyūsha) |
GOTO Jun 東京大学, 医学部附属病院, 講師 (10211252)
TAKAHASHI Yuji 東京大学, 医学部附属病院, 助教 (00372392)
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| Project Period (FY) |
2005 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥781,600,000 (Direct Cost: ¥781,600,000)
Fiscal Year 2009: ¥156,400,000 (Direct Cost: ¥156,400,000)
Fiscal Year 2008: ¥156,200,000 (Direct Cost: ¥156,200,000)
Fiscal Year 2007: ¥161,700,000 (Direct Cost: ¥161,700,000)
Fiscal Year 2006: ¥163,400,000 (Direct Cost: ¥163,400,000)
Fiscal Year 2005: ¥143,900,000 (Direct Cost: ¥143,900,000)
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| Keywords | ゲノム / 脳神経疾患 / 遺伝子 / 遺伝学 / 脳・神経 / 分子遺伝学 / 多型解析 / 神経変性疾患 / 脊髄小脳変性症 / 脳血管障害 / 連鎖漢籍 / 相関解析 / 連鎖解析 |
|---|
| Research Abstract |
This study has focused on elucidation of molecular mechanisms of neurological diseases based on genome analysis, and, eventually, to develop disease-modifying therapy for neurological diseases. This study focused on the broad range of neurological diseases ranging from single gene diseases to polygenic diseases. To facilitate the linkage study for familial diseases, a high throughput linkage analysis system (SNP HiTLink) employing SNP microarrays has been developed and applied for many diseases. Regarding single gene diseases, we have discovered the causative gene for cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL). For sporadic diseases, we have identified a strong disease suseceptibility gene for Parkinson disease. The result emphasizes the paradigm shift from common disease-common variants hypothesis to common disease-multiple rare variants hypothesis.
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