A novel model for DNA damageaccumulation in Alzheimer's disease
| Project/Area Number |
17K16113
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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 | The University of Tokyo |
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Principal Investigator |
Mano Tatsuo 東京大学, 医学部附属病院, 助教 (20704331)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アルツハイマー病 / DNA傷害 / ３次元細胞培養系 / アミロイドβ / リン酸化タウ / 剖検脳 / 神経細胞 / 細胞モデル / 三次元培養 / 脳神経疾患 |
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| Outline of Final Research Achievements |
In the early stage of Alzheimer's disease, amyloid beta induced DNA damages in neuronal cells, which are repaired by BRCA1. However, these mechanism was deteriorated by BRCA1 co-aggregation with phosphorylated tau in the advanced stage of Alzheimer's disease. We developed a novel model for DNA damage accumulation in neuronal cells. We also developed a method for quantification of DNA damage accumulation using FACS, and analyzed genome-wide distribution of DNA damages and BRCA1 binding regions.
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| Academic Significance and Societal Importance of the Research Achievements |
アルツハイマー病の病態はいまだ明らかでなくが、今回の研究では神経細胞におけるDNA傷害の蓄積が神経細胞の機能低下の一因となっている可能性を示し、細胞モデルの構築を行った。さらにはゲノム上のDNA傷害領域、修復タンパクの結合領域を解析した。DNA傷害・修復は神経細胞における普遍的な問題であると考えられ、本研究はアルツハイマー病の病態とともに、加齢における神経細胞の変化についても明らかにしてければと考えている。
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Report
(3 results)
Research Products
(22 results)
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[Journal Article] Case of a 78-year-old woman with a neuronal intranuclear inclusion disease.2017
Author(s)
Takumida H, Yakabe M, Mori H, Shibasaki K, Umeda-Kameyama Y, Urano T, Mano T, Hayashi A, Ikemura M, Ogawa S, Akishita M.
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Journal Title
Geriatr Gerontol Int
Volume: 17
Issue: 12
Pages: 2623-2625
DOI
Related Report
Peer Reviewed
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