Demyelination: a failure of cell communication?
A hypothesis is proposed that demyelination in both the CNS and PNS involves a failure of cell communication between the axon and oligodendrocyte/Schwann cell, as a primary event. The site of communication is assumed to be the paranodal myelin loop-axolemma membrane complex. It is postulated that "cross-talk" between the two cell types can be interrupted, and hence demyelination initiated, by pathophysiological changes in either the axon or myelinating cell. Experimental evidence in support of the hypothesis is cited in so far as it exists.
D001370:Axonal Transport; D001369:Axons / Q000648:ultrastructure; D002450:Cell Communication; D003711:Demyelinating Diseases / Q000473:pathology*; D006801:Humans; D009186:Myelin Sheath / Q000648:ultrastructure; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009836:Oligodendroglia / Q000648:ultrastructure; D011901:Ranvier's Nodes / Q000648:ultrastructure; D012583:Schwann Cells / Q000648:ultrastructure
D009419:Nerve Tissue Proteins