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  1. 020 学位論文
  2. 生命科学研究科
  3. 20 生理科学専攻

Glial cell activation and re-expression of putative myelinating inhibitors in the brain of mouse model for demyelinating disease

https://ir.soken.ac.jp/records/1148
https://ir.soken.ac.jp/records/1148
ab5853ee-1d70-485b-9e78-6195c06b7e78
名前 / ファイル ライセンス アクション
甲784_要旨.pdf 要旨・審査要旨 / Abstract, Screening Result (183.1 kB)
甲784_本文.pdf 本文 (1.4 MB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2010-02-22
タイトル
タイトル Glial cell activation and re-expression of putative myelinating inhibitors in the brain of mouse model for demyelinating disease
タイトル
タイトル Glial cell activation and re-expression of putative myelinating inhibitors in the brain of mouse model for demyelinating disease
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_46ec
資源タイプ thesis
著者名 松本, 路生

× 松本, 路生

松本, 路生

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フリガナ マツモト, ミチオ

× マツモト, ミチオ

マツモト, ミチオ

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著者 MATSUMOTO, Michio

× MATSUMOTO, Michio

en MATSUMOTO, Michio

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学位授与機関
学位授与機関名 総合研究大学院大学
学位名
学位名 博士(理学)
学位記番号
内容記述タイプ Other
内容記述 総研大甲第784号
研究科
値 生命科学研究科
専攻
値 20 生理科学専攻
学位授与年月日
学位授与年月日 2004-03-24
学位授与年度
値 2003
要旨
内容記述タイプ Other
内容記述 Overexpression of the proteolipid protein (PLP) gene, which is the major component of central nervous system myelin, causes unique demyelinating disorder in mice(Plp/- mouse). In this transgenic animal model, normal-appearing myelin is formed at an early stage of their life and late-onset chronic demyelination occurs after several months. I aimed to understand the molecular mechanisms underlying this neuropathology. I first demonstrated that remyelination is severely affected in the aged Plp/- mouse. This was not caused by the deprivation of oligodendrocyte progenitors, expressing Olig1, Olig2 and Sox10, because they were present at a higher number in the central nervous system of mutant mice than in the wild type control throughout their lives. These suggested that oligodendrocyte progenitors cannot differentiate or mature due to a change in the microenvironment. I then searched for factors inhibiting oligodendrocyte development. I observed up-regulation of PSA-NCAM and cystatin C expression, both of which have been reported to be inhibitory for oligodendrocyte development and are produced by nonoligodendroglial cells. Thus I investigated the change in the number and properties of astrocytes and microglia. Glial activation was observed much earlier than the active demyelinating period. These data imply that not only cell intrinsic mechanisms but also extrinsic mechanisms contribute to the defect in re-myelination in the PLP overexpressing brain. During demyelination, resident microglial cells and astrocytes become activated, astrogliosis occurs, and these cells may change the environment to that inhibitory for oligodendrocyte differentiation/maturation.
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内容記述 application/pdf
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