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Demyelinating Disorders

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

CNS myelin morphology in the acute phase of experimental autoimmune encephalomyelitis

  • P1-328
  • 板東 良雄 / Yoshio Bando:1 暮地本 宙己 / Hiroki Bochimoto:2 村上 公一 / Koichi Murakami:1 田中 達英 / Tatsuhide Tanaka:1 渡部 剛 / Tsuyoshi Watanabe:2 吉田 成孝 / Shigetaka Yoshida:1 
  • 1:旭川医科大学 / Dept Functional Anatomy and Neuroscience, Asahikawa Medical Univ, Hokkaido, Japan 2:旭川医科大学 解剖学講座 顕微解剖学分野 / Dept Microscopic Anatomy and Cell biology, Asahikawa Medical Univ, Hokkaido, Japan 

Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the CNS. Demyelination and axonal damage are responsible for neurological deficits in MS. However, the mechanisms of demyelination and axonal damage have not been fully understood. To clarify the mechanism of demyelination in experimental autoimmune encephalomyelitis (EAE), we examined myelin morphology during the course of MOG35-55-induced EAE in the C57BL/6 mice. Here we used osmium-maceration scanning electron microscopic (SEM) analysis.
Osmium-maceration SEM analysis displayed clear variations in the ultrastructural abnormalities of myelin structure in the white matter of the EAE spinal cord. For example, myelin detachment and excess myelin formation were observed as typical abnormalities of myelin during demyelination in EAE. Importantly, compact myelin was well preserved even though in these situations.
We also found that myelin detachment from the axon was observed at early stages of EAE. At this point, infiltrating immune cells into the CNS were not observed in the spinal cord. These observations suggest that non-inflammatory demyelination in the acute phase of EAE plays an important role in the pathogenesis of EAE.

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