Copper chelation and autoimmunity differentially impact myelin in the hippocampal-prefrontal circuit.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. About 50% of MS patients develop deficits in learning, memory and executive function, which are accompanied by demyelinating lesions in the hippocampus and/or prefrontal cortex (PFC). Why demyelination in these regions occurs in some patients but not in others and what is the underlying mechanism remain unclear. Here we report that myelin density in the hippocampus and PFC is markedly reduced in the cuprizone model, but not in the chronic experimental autoimmune encephalomyelitis. These two models can be used for studying different neuropathophysiological aspects of demyelinating diseases.