Investigation of contribution of novel tight junction molecule at the two big central nervous system barriers and its usefulness as a therapeutic target for multiple sclerosis

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15475
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Neurology
• Research Institution: Tohoku University
• Principal Investigator: Uchida Yasuo 東北大学, 薬学研究科, 助教 (70583590)
• Co-Investigator(Renkei-kenkyūsha): TACHIKAWA Masanori 東北大学, 大学院薬学研究科, 准教授 (00401810) ; TERASAKI Tetsuya 東北大学, 大学院薬学研究科, 教授 (60155463)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: Claudin-11 / 多発性硬化症 / 血液脳関門 / 血液脊髄関門 / 血液脳脊髄液関門 / 血液クモ膜関門 / 定量プロテオミクス / 密着結合

Outline of Final Research Achievements

Multiple sclerosis is a disorder that autoreactive lymphocytes invade into central nervous system (CNS) and destroy it. The inhibition of disruption of the CNS barriers (which allows the lymphocytes invade into the CNS) is an important therapeutic strategy. However, it remained to be elucidated for the molecular mechanism of CNS barrier breakdown. The present study was the first to clarify that “claudin-11” contributes to the tight junction formation of several CNS barriers and its down-regulation causes the breakdown of CNS barriers in multiple sclerosis.

Free Research Field

中枢関門科学