We are using a mouse model where oligodendrocytes are specifically deleted after induced expression of diptheria toxin receptors combined with our NG2-EYFP knockin mouse to study the response of NG2+ glia to demyelination and their role in remyelination. We hope to shed light on the failed remyelination seen in chronic lesions of Multiple Sclerosis, where in spite of the presence of NG2+ cells remyelination appears to be blocked.
Funding
DFG
