Examples of demyelination

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Insights into axonal pathology as well as grey matter demyelination raised the attention to the significance of grey matter pathology.
We found that cells accumulate in the white matter of plptg/- mice as demyelination progresses (data not shown).
An attractive way to repair the damage caused by oligodendrocyte death and demyelination is to harness and amplify the endogenous regenerative response to injury.
We defined the disease duration as the number of months since the first clinical identification of demyelination.
Interestingly, most animal models of demyelination show high levels of spontaneous remyelination.
Thus, there is a parallel relationship between the density of microglia/brain macrophages increase and demyelination progression.
This makes them an ideal model to study the time-course of demyelination because progression is unidirectional.
We achieve this by comparing nodal clustering of ion channels in the presence and absence of oligodendrocytes in two in vivo models of demyelination.
It is important to note that the loss of oligodendrocytes precedes the initiation of demyelination by 2 weeks.
Demyelination and axonopathy were observed only within inflammatory foci.
Glial activation also occurred much earlier than active demyelination in mutant mice.
This loss occurs before demyelination and appreciable structural changes in the myelin sheath, but corresponds precisely with the loss of oligodendrocytes.
We first examined the cells that react during the course of demyelination.

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