The Authors treated parenterally albino rats with organic salt and sodium azide; the latter in order to prevent the copper chelation by seric céruloplasmine and to maintain a high level of free hematic copper. Within 30 days such a treatment to a status spongiosus of white matter, Alzheimer's II glia production, focus of fat granule cells and proliferation of capillaries. As these lesions are peculiar to human Wilson disease the treatment in question may be considered as a valid experimental model. The Authors discuss the meaning of these observations in copper neurobiology and in the pathogenesis of Wilson's disease.
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