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Wilson disease is a congenital disorder of copper metabolism whose pathogenesis remains, al least in part, unknown. Subjects carrying the same genotype may show completely different phenotypes, differing for the age at illness onset or for the hepatic, neurologic or psychiatric clinical presentation. The inhability to find a unequivocal correlation between the type of mutation in the ATPase copper transporting beta (ATP7B) gene and the phenotypic manifestation, induced
many authors to look for epigenetic factors interacting with the genetic changes. Here the evidences regarding the ability of
copper overload to change the global DNA methylation status are discussed.
Congenic strains displaying similar clinical phenotype of arthritis represent different immunologic models of inflammation
