脱髄とカルパイン

Calpain in demyelination.

はじめに

　多発性硬化症に代表されるヒトの脱髄性疾患の病態生理には，免疫学的機序が考えられるが，分子レベルでの脱髄のメカニズムは明らかではない。1970年代より，脱髄におけるプロテアーゼの重要性が注目され，これまで多くの研究が進められてきた。

　本稿においては，プロテアーゼの中でもカルパインを中心に髄鞘タンパクの分解作用および多発性硬化症における動態に関し概説する。

It has been well established that myelinproteins and lipids are substantially reduced in demyelinating disorders. However, the molecular mechanism of demyelination has not been elucidated. The beneficial effects of protease inhibitor in experimental allergic encephalomyelitis, which is an animal model of multiple sclerosis, indicates the involvement of proteases in demyelinating processes. From previous bio-chemical studies, it has been suggested that myelin membranes contain an endogenous neutral protease that degrades myelin basic protein (MBP) and myelin-associated glycoprotein (MAG) (Sato et al., 1982).