A low blood copper concentration is a co-morbidity burden factor in Parkinson’s disease development

Parkinson’s disease (PD) patients are often characterized by copper dyshomeostasis, which is responsible for ROS formation and fibrillogenesis. However, the relationships between copper metabolism and PD development are unclear. In this study in 50 patients with PD (pPD) and 50 age-matched healthy i...

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Bibliographic Details
Published in:Neuroscience research 2018-10, Vol.135, p.54-62
Main Authors: Ilyechova, Ekaterina Y., Miliukhina, Irina V., Orlov, Iurii A., Muruzheva, Zamira M., Puchkova, Ludmila V., Karpenko, Marina N.
Format: Article
Language:English
Subjects:
Aged
Blood serum copper
Ceruloplasmin
Ceruloplasmin - metabolism
Ceruloplasmin labile copper atoms
Copper - blood
Female
Humans
Interleukin-6
Interleukin-6 - blood
Interleukin-6 - metabolism
Male
Middle Aged
Parkinson Disease - blood
Parkinson Disease - enzymology
Parkinson’s disease
SOD3
Superoxide Dismutase - blood
Superoxide Dismutase - metabolism
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Summary:Parkinson’s disease (PD) patients are often characterized by copper dyshomeostasis, which is responsible for ROS formation and fibrillogenesis. However, the relationships between copper metabolism and PD development are unclear. In this study in 50 patients with PD (pPD) and 50 age-matched healthy individuals, the serum total copper concentration, oxidase activity, ceruloplasmin and SOD3 protein concentrations were measured; and amount of copper atoms per ceruloplasmin molecule was calculated. These parameters were lower in pPD relatively to healthy volunteers. Decrease in concentrations of SOD3, ceruloplasmin, and copper but increase of interleukin-6 levels were associated with a risk of PD. Two consistent patterns were identified. First, a low serum copper concentration related with PD development and predominantly affected the non-motor symptoms of PD. There was no correlation between copper concentration and ceruloplasmin oxidase activity level (r = 0.27) in pPD. Second, Chelex 100 treatment revealed that pPD ceruloplasmin compared with ceruloplasmin of healthy individuals displayed smaller content of labile copper atoms. The presence or absence of these atoms had no effect on ceruloplasmin enzymatic activities. Our findings suggest that cuproenzyme deficiency, which is typical for PD, can be caused by violation of metabolic incorporation of the labile copper atoms into ceruloplasmin molecule.
ISSN:0168-0102
1872-8111
DOI:10.1016/j.neures.2017.11.011