2018 Fiscal Year Final Research Report
Investigation of novel cellular function of Progranulin and its molecular mechanism
Project/Area Number |
16K08557
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
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Research Institution | Tokyo Medical University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 神経変性疾患 / 神経細胞死 |
Outline of Final Research Achievements |
Dysfunction of Progranulin by gene mutation is thought to cause Frontotemporal dementia. However, its molecular mechanism is still not well understood, and the progranulin receptor involved in the onset is also unknown. In this study, I attempted to identify Pogranulin receptors and binding molecules involved in the onset of FTD, and found some novel binding partners. Furthermore, interaction with Progranulin induced lysosomal degradation of these binding molecules. These results suggest that Progranulin may be involved in neuroprotective function control via these new binding molecules.
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Free Research Field |
薬理学
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Academic Significance and Societal Importance of the Research Achievements |
前頭側頭型認知症(FTD)をはじめとする神経変性疾患において、これまでに研究により複数の原因遺伝子が同定されているが、その発症メカニズムには未だ不明な点が多く残されている。このため、本研究で同定したProgranuliin結合分子は、発症メカニズム解明の一助となることが期待される。また、Progranulinは、近年、FTDだけでなくアルツハイマー病(AD)やパーキンソン病(PD)の発症にも関わると報告されており、本研究成果はFTDのみならず、ADやPDなどの神経変性疾患の根本的治療法および治療薬の開発の基盤となることが予想される。
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