The myelin sheath, a lipid-rich multilamellar membrane of relative sta
bility, both insulates and enhances conduction in nerve axons. A notab
le feature of myelin-specific proteins, in particular myelin basic pro
tein, is their susceptibility to proteolytic activity and their enceph
alitogenicity, which induces inflammatory demyelination in the CNS. Th
e final common pathway of myelin breakdown in vivo is well documented
and there is evidence that myelin disruption can be mediated directly
by soluble (circulating) factors and for following receptor-driven pha
gocytosis by macrophages. However the exact mechanism(s) of demyelinat
ion in multiple sclerosis is still unresolved, both antigen-specific a
nd - non-specific events having the potential to generate the myelinol
ytic process.