Albumin protects human red blood cells against Aβ25-35-induced lysis more effectively than ApoE

Luciano Galeazzi, Roberta Galeazzi, M. Beatrice Valli, Elizabeth H. Corder, Sergio Giunta

Research output: Contribution to journalArticlepeer-review

Abstract

Inhibition of the lysis of human red blood cells (RBCs) exposed to amyloid peptide Aβ25-35 is an in vitro model for screening natural and synthetic substances potentially protective against amyloid damage. In this system, human serum and a component, namely apolipoprotein E (apoE), completely prevent RBC lysis. This report demonstrates that albumin, another serum component, is 8-fold more protective: a concentration of 12.5 μg/ml protects RBCs against 20μM-Aβ25-35, and prevents the formation of fibrillar Aβ25-35 aggregates stainable by Congo Red. The biological relevance of these findings is suggested by the following: (1) a large fraction (∼90%) of circulating Aβ1-42 is bound to albumin; (2) albumin immunoreactivity is present in brain amyloid plaques; and (3) incubation of Aβ with albumin rapidly decreases detectable levels of free Aβ suggesting epitope masking. The results add new and important functional consequences to the amyloid-albumin relationship and imply that experimental systems investigating Aβ cytotoxicity should consider the protective interaction of albumin.

Original languageEnglish
Pages (from-to)2149-2154
Number of pages6
JournalNeuroReport
Volume13
Issue number16
DOIs
Publication statusPublished - Nov 15 2002

Keywords

  • Albumin
  • Alzheimer pathogenesis
  • Amyloid-β
  • ApoE
  • Drug screening
  • In vitro models
  • Red blood cells

ASJC Scopus subject areas

  • Neuroscience(all)

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