There is also a non-autoimmune approach to demyelinating neurons in animal models. Cuprizone is a toxin that can be injected as a way of killing oligodendrocytes and simulating the neuropathology of demyelination. Though this approach does not induce an auto-immune effect like EAE, it does generate an inflammatory response that is associated with MS pathology. After treatment is ended myelin will be restored after 3-6 weeks, as OPC's that survive the treatment repopulate the region of insult. There is controversy in the field over what model best suits MS research (see second link). It really depends on what effect your intervention is hypothesized to demonstrate. It is important to carefully sort out the intentions of your study before selecting your model. See the link below for a helpful review of the Cuprizone model, and the other for a debate over MS models in general:
Article Cellular and molecular neuropathology of the cuprizone mouse...
There is also a non-autoimmune approach to demyelinating neurons in animal models. Cuprizone is a toxin that can be injected as a way of killing oligodendrocytes and simulating the neuropathology of demyelination. Though this approach does not induce an auto-immune effect like EAE, it does generate an inflammatory response that is associated with MS pathology. After treatment is ended myelin will be restored after 3-6 weeks, as OPC's that survive the treatment repopulate the region of insult. There is controversy in the field over what model best suits MS research (see second link). It really depends on what effect your intervention is hypothesized to demonstrate. It is important to carefully sort out the intentions of your study before selecting your model. See the link below for a helpful review of the Cuprizone model, and the other for a debate over MS models in general:
Article Cellular and molecular neuropathology of the cuprizone mouse...