Cuprizome is a copper chelator and subsequent copper deficit alters mitochondrial function in the brain and induces disturbance of energy metabolism in oligodendroglia leading to apoptosis. The selective vulnerability of oligodendroglia has been linked to myelin synthesis which requires vast amounts of energy.
You might also like having a look at this review article:
Cuprizone-induced demyelination as a tool to study remyelination and axonal protection http://www.ncbi.nlm.nih.gov/pubmed/23666824
Check our recent paper on cuprizone induced demyelination in mice. As mentioned above by Norbert, the prevailing view is that it causes starvation of oligodendrocytes. However, the true story is likely to be more complicated than that. There seems to be a gender- and strain -dependence of its demyelinating effects, with mechanisms largely unknown.