Ceruloplasmin fragmentation is implicated in 'free' copper deregulation of Alzheimer's disease.

Rosanna Squitti, Carlo C. Quattrocchi, Carlo Salustri, Paolo M. Rossini

Research output: Contribution to journalArticlepeer-review

Abstract

A dysfunction in copper homeostasis seems to occur in Alzheimer's disease (AD). We recently demonstrated that an excess of non-ceruloplasmin-copper (i.e., 'free' copper) correlates with the main functional and anatomical deficits as well as the cerebrospinal markers of the disease, thus suggesting that copper contributes to AD neurodegeneration. Aim of this study was to investigate the profile of serum ceruloplasmin isoforms immunoreactive protein in relation to copper dysfunction in AD. Twenty-five AD patients and 25 controls were included in the study. All subjects underwent individual measurements of serum ceruloplasmin and copper concentrations, and the amount of 'free' copper was computed for each copper and ceruloplasmin pair. Serum samples were also pooled and analyzed by two dimensional polyacrylamide gel electrophoresis (2-D PAGE) and western blot analysis. The mean concentration of 'free' copper resulted higher in AD patients than in controls. Ceruloplasmin 2-D PAGE western blot analysis of pooled sera showed in the AD samples low-molecular-weight spots in the

Original languageEnglish
Pages (from-to)23-27
Number of pages5
JournalPrion
Volume2
Issue number1
Publication statusPublished - Jan 2008

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Infectious Diseases
  • Cellular and Molecular Neuroscience

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