Analysis of axonal vulnerability in immune-mediated demyelination: a role of TAG-1 for remyelination.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461278
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurology
• Research Institution: Nagoya University
• Principal Investigator: IIJIMA MASAHIRO 名古屋大学, 医学(系)研究科(研究院), 寄附講座講師 (40437041)
• Co-Investigator(Kenkyū-buntansha): Sobue Gen 名古屋大学, 医学系研究科, 特任教授 (20148315) ; Kawagashira Yuichi 名古屋大学, 医学部附属病院, 病院助教 (40569779) ; Koike Haruki 名古屋大学, 医学系研究科, 准教授 (80378174)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 免疫介在性ニューロパチー / TAG-1 / 傍ランビエ絞輪部 / 脱髄 / 軸索障害 / 動物モデル / 免疫性疾患 / 脳神経疾患

Outline of Final Research Achievements

Interaction between axon and myelin sheath has a crucial role for the maintenance of the peripheral nervous system. We have clarified that TAG-1, which specifically distributes on juxtaparanode, ameliorates the remyelinating process depends on non-synonymous amino acids changes through SNPs. In this study, we produce an experimental autoimmune neuritis model by inducing myelin-origined peptides with complete Freund adjuvant. This mice showed inflammatory demyelination followed by severe axonal degeneration. TAG-1 could work as a trigger for remyelination after demyelination. In addition, dysfunction of juxtaparnodal molecules would bring severe irreversible pathogenesis as like axonal degeneration.

Free Research Field

免疫性神経疾患