MRI analysis of experimental multiple sclerosis animal models.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591261
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurology
• Research Institution: National Institute for Physiological Sciences (2014); Osaka University (2012-2013)
• Principal Investigator: FUKUNAGA MASAKI 生理学研究所, 大脳皮質機能研究系, 准教授 (40330047)
• Co-Investigator(Kenkyū-buntansha): MORI Yuki 大阪大学, 免疫学フロンティア研究センター・生体機能イメージング, 特任助教 (10559355) ; MORITA Masashi 大阪大学, 免疫学フロンティア研究センター・生体機能イメージング, 特任助教 (30381594)
• Co-Investigator(Renkei-kenkyūsha): YOSHIOKA Yoshichika 大阪大学, 免疫学フロンティア研究センター・生体機能イメージング, 特任教授 (00174897)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 多発性硬化症 / MRI / 脱髄 / マンガン造影

Outline of Final Research Achievements

Multiple sclerosis (MS) is one of the most common autoimmune diseases of the central nervous system (CNS). Cuprizone is a mitochondrial toxin that induces demyelination in the CNS, and is used for animal model in MS. In this study, we investigated Manganese enhanced MRI (MEMRI) in cuprizone induced demyelinated mouse brain using 11.7T MRI, and analyzed with histology and glial marker expressions. Conventional T2 weighted images show hyperintense in corpus callosum, and its size was increased up to 5th week. In MEMRI, positive signal enhancement in corpus callosum was observed at 3rd week, but the signal strength had a tendency to peaking at 4th weeks and reducing to 5th weeks. In RT-PCR, GFAP expression was monotonically increased to 5th week, however Iba-1 expression showed peak at 3rd week and diminished at 5th week, that was similar as MEMRI enhancement. In conclusion, MEMRI may reflect phenomenon accompanying microglia activation on the cuprizone induced demyelination.

Free Research Field

磁気共鳴医学