Abstract
Multiple Sclerosis (MS) is characterized by the presence of demyelinating lesions in the Central Nervous System (CNS). The demyelination is accompanied by axonal degeneration and the activation of cells of the innate and adaptive immune systems that accumulate around the demyelinated plaques. Oligodendrocyte cell dysfunction and death are also evident. In the relapsing-remitting form of MS, this dysfunction is followed by periods of recovery, and newly mature oligodendrocytes have the ability to remyelinate the pathological axons. To specifically study the localized demyelination/remyelination processes, animal models involving specific demyelinating toxins or viruses have been generated. Through these models the pathological effects on oligodendrocytes can be analyzed, and pharmacological treatments that can restore oligodendrocyte myelination capabilities can be assessed. Here we describe the most commonly used models of toxic or viral demyelination, and provide protocols to induce and analyze them.
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