Treatment strategy of Lewy body disease by activation of intracellular degradation system

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860655
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurology
• Research Institution: Hirosaki University
• Principal Investigator: Miki Yasuo 弘前大学, 医学(系)研究科(研究院), 助教 (30709142)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: レビー小体病 / α-シヌクレイン / オートファジー / トレハロース / Beclin1

Outline of Final Research Achievements

The accumulation of mis-folded and/or abnormally modified proteins is a major characteristic of many neurodegenerative diseases. In Lewy body disease (LBD), insoluble α-synuclein is widely deposited in the presynaptic terminals as well as in the neuronal cytoplasm in distinct brain regions. The autophagy-lysosome system is an efficient degradation pathway for abnormal molecules within cells. We investigated the effect of trehalose on abnormal aggregation of α-synuclein in a model of LBD. Trehalose treatment induced autophagy and reduced level of detergent-insoluble α-synuclein, although an apparent alteration was not observed in abnormal aggregation of α-synuclein. These results indicate that the oral intake of trehalose can be a promissing treatment for prevention of accumulation of abnormal α-synuclein, especially before aggregation formation.

Free Research Field

神経内科