Role of Copper Dyshomeostasis in the Pathogenesis of Parkinson’s Disease

Abstract

Serum concentration of copper, immunoreactive polypeptides of ceruloplasmin and its oxidase activity, and the number of copper atoms per ceruloplasmin molecule were decreased in patients with Parkinson’s disease in comparison with the corresponding parameters in age-matched healthy individuals, but the ratio of apoceruloplasmin to holoceruloplasmin in patients with Parkinson’s disease was similar in both groups. Treatment of blood serum with Helex 100, a high-affinity copper chelator, revealed reduced content of labile copper atoms per ceruloplasmin molecule in patients with Parkinson’s disease in comparison with that in healthy controls. The mechanism underlying impaired metabolic incorporation of labile copper atoms into CP molecule is discussed as a possible cause of copper dyshomeostasis associated with Parkinson’s disease.