Analysis of the pathomechanism of secondary demyelination in primary astrocytopathy model

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591247
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurology
• Research Institution: Tohoku University
• Principal Investigator: MISU Tatsuro 東北大学, 医学(系)研究科(研究院), 助教 (00396491)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 神経免疫 / 脱髄 / アストロサイト / アクアポリン

Outline of Final Research Achievements

Neuromyelitis optica (NMO) is an autoimmune inflammatory disease by anti-aquaporin 4 (AQP4) antibody mainly targeting against astrocyte foot processes in the central nervous system (CNS). However, the mechanism of demyelination is not well resolved.
In this project, we have studied the mechanism of astrocytopathy and demyelination by passive transfer model of AQP4 antibody on rodent experimental encephalomyelitis. This model is featured by highly reproducible and typical astrocytopathy lesion like post-mortem cases of NMO. It is revealed that demyelination is secondarily produced after the induction of astrocytopathy lesion, and the lesion development is higly associated with infiltration of inflammatory cells, especially neutrophil.

Free Research Field

神経内科学