1AFaR, Dept. of Neuroscience, Fatebenefratelli Hospital, Rome, Italy. 2Depts. of Radiology "Campus Biomedico" University, Rome, Italy. 3Depts. of Neurology, "Campus Biomedico" University, Rome, Italy. 4Dept. of Neurology, Medical College of Wisconsin, Milwaukee, WI, U.S.A. 5University of Kentucky Alzheimer's Disease Research Center, Lexington, KY, U.S.A. 6Dept. of Biology, Tor Vergata University, Rome, Italy. 7Institute of Cognition Sciences and Technologies (CNR), Rome, Italy. 8IRCCS ‘Centro S. Giovanni di Dio-FBF', Brescia, Italy.
Abstract: A dysfunction in copper homeostasis seems to occur in Alzheimer's disease (AD). We previously evidenced that an excess of non-ceruloplasmin-copper (NCC) correlated with the main functional, anatomical as well as cerebrospinal markers of the disease. Aim of our study was to investigate ceruloplasmin isoforms as potential actors in this AD copper dysfunction. Our data show that AD patients have ceruloplasmin fragments of low molecular weight (<50 kDa) both in their serum and brain, contrary to healthy controls. Ceruloplasmin isoforms of higher molecular weight (115 and 135 kDa in serum and 135 kDa in brain), as well as copper levels in the brain, instead, do not seem to mark a difference between AD and healthy subjects. These data suggest a ceruloplasmin fragmentation in the serum of AD patients. Some clues in this direction have been found also in the AD brain.
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