chemical biology for cytosolic amyloid beta

2018 Fiscal Year Final Research Report

• Project/Area Number: 17K19476
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Research Field: Pharmaceutical Sciences and related fields
• Research Institution: The University of Tokyo
• Principal Investigator: Ishikawa Minoru 東京大学, 定量生命科学研究所, 准教授 (70526839)
• Project Period (FY): 2017-06-30 – 2019-03-31
• Keywords: 神経変性疾患

Outline of Final Research Achievements

Neurodegenerative disorders, such as Alzheimer's disease, and Parkinson's disease ( are caused by aggregates of misfolded proteins including amyloid beta and alpha synuclein. We had shown that small hybrid molecules by linking a ligand for ubiquitin ligase with probes for aggregates induce selective degradation of mutant huntingtin. Here, we aimed at decrease of other aggregation-prone proteins that induce neurodegenerative disorders. As a result, we discovered a small molecule that induce decrease of apha synulein in living cells.

Free Research Field

創薬化学

Academic Significance and Societal Importance of the Research Achievements

65歳以上の約7人に1人が認知症と推計されており、この対策が本国にとっても最重要課題のひとつである。今回、認知症の原因となる凝集性タンパク質の存在量を減少させる低分子を創製した。本発見は、認知症に対する新しい創薬手法に繋がる可能性がある。