| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
We have shown the effect of COX2-inhibitor in the treatment of an experimental allergic neuritis (EAN), an animal model of immune-mediated neuropathy. It acts on effector phase of pathological process, a macrophage-mediated nerve damage. It is unique in the point that COX-2 inhibitor is effective even after the onset of neurological symptoms. Next, we examinedthe expression of COX-2 in human biopsied nerve. In chronic inflammatory demyelinating polyneuropathy (CIDP), the macrophage of COX-2 positivity was accepted in accordance with the actively demyelinating lesion. Moreover, the increase in m-RNA level was confirmed. Therefore, COX-2-inhibitor may be one of the choices of treatment in CIDP.
It is not yet clear that an auto-antibody is associated with the pathogenesis of CIDP. In one case, the anti-galactocerebroside antibody was increased and fell down in proportion with an improvement of symptoms. Nerve biopsy showed an uncompaction of myelin which suggested the significance of the antibody.
The spectrum of polyneuropathy is various and there are not especially few patients with poor prognosis. In this case, the interruption of the cell cycle of a Schwann cell and the stop of multiplication would be concerned. We examined about neuregulin which attracts attention as an axon-derived trophic factor. Consequently, neuregulin-beta 1 was intensely expressed in axons that were actively showing degeneration or in regenerating axons. On the other hand, there was almost no expression in chronic stages of axonal loss. When neuregulin could be introduced by a certain method, dedifferentiation of a Schwann cell were caused that follow nerve reproduction.
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