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NEUROLOGY 2005;64:1040-1046
© 2005 American Academy of Neurology

Excess of serum copper not related to ceruloplasmin in Alzheimer disease

R. Squitti, PhD, P. Pasqualetti, PhD, G. Dal Forno, MD, PhD, F. Moffa, PhD, E. Cassetta, MD, D. Lupoi, MD, F. Vernieri, MD, L. Rossi, PhD, M. Baldassini, MD and P. M. Rossini, MD

From the Departments of Neuroscience (Drs. Squitti, Pasqualetti, Dal Forno, Moffa, Cassetta, Vernieri, and Rossini), Radiology (Dr. Lupoi), and Laboratory Medicine (Dr. Baldassini), AfaR–Osp. Fatebenefratelli Rome; Clinica Neurologica (Drs. Dal Forno and Rossini), Università Campus Biomedico, Rome; Department of Biology (Dr. Rossi), Tor Vergata University, Rome; and IRCCS ‘Centro S. Giovanni di Dio-FBF’ (Dr. Rossini), Brescia, Italy.

Address correspondence and reprint requests to Dr. Rosanna Squitti, Department of Neuroscience, AFaR–Osp. Fatebenefratelli, 00186, Rome, Italy; e-mail: rosanna.squitti{at}afar.it

Objective: To assess the role of serum copper in relation to ceruloplasmin and other peripheral markers of inflammation in Alzheimer disease (AD).

Methods: The authors studied serum levels of copper, ceruloplasmin, and transferrin, as well as total peroxides, antioxidants, and other peripheral markers of inflammation in 47 patients with AD, 24 patients with vascular dementia (VaD), and 44 healthy controls. Biochemical variables were related to the patients’ and controls’ clinical status.

Results: The authors found that copper (p < 0.001), peroxides (p = 0.026), and ceruloplasmin (p = 0.052) were increased and TRAP was decreased (p = 0.006) in patients with AD, while no other markers of inflammation were altered. The calculation of the ratio between copper and ceruloplasmin suggested the presence in the serum of AD patients, but not of VaD or normal controls, of a large pool of non-ceruloplasmin-bound copper.

Conclusions: Changes in the distribution of the serum copper components, consisting of an increase of a copper fraction not explained by ceruloplasmin, seem to be characteristic of Alzheimer disease and may be implicated in the pathogenesis of the disease.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 22 issue to find the title link for this article.

Supported by grants from ISPSL, PFA/DML/UO5/2001/AA "Malattia di Alzheimer: studio del rischio legato a fattori lavorativi," and by a grant from AFaR Foundation–Osp. Fatebenefratelli Rome, Italy.

Received May 13, 2004. Accepted in final form November 19, 2004.




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Excess of serum copper not related to ceruloplasmin in Alzheimer disease
Steven R Brenner
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