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2014 Fiscal Year Final Research Report

Investigation for a New Mechanism of Demyelination in Demyelinating Model Mice

Research Project

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Project/Area Number 24500404
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Nerve anatomy/Neuropathology
Research InstitutionAsahikawa Medical College

Principal Investigator

YOSHIDA Shigetaka  旭川医科大学, 医学部, 教授 (20230740)

Co-Investigator(Kenkyū-buntansha) BANDO Yoshio  旭川医科大学, 医学部, 准教授 (20344575)
TANAKA Tatsuhide  旭川医科大学, 医学部, 助教 (80567032)
MURAKAMI Koichi  旭川医科大学, 医学部, 助教 (90400085)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords脱髄 / オリゴデンドロサイト / 多発性硬化症 / EAE / プロテアーゼ
Outline of Final Research Achievements

The objective of the current study was to elucidate the mechanism of demyelination from the change of myelin condition and the function of the protease of oligodendrocytes. In experimental autoimmune allergic encephalitis, changes of the condition of myelin occurred earlier than previously thought. The involvement of KLK6 was also suggested. In contrast, demyelination by cuprizone administration was caused by different mechanism with less involvement of KLK6. KLK6 was also partially involved in demyelination after spinal cord injury. From the study of cultured oligodendrocytes, KLK6 may play a role during demyelination rather than development of oligodendrocytes.

Free Research Field

神経解剖学

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Published: 2016-06-03  

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