Enhanced binding of advanced glycation endproducts (AGE) by the ApoE4 isoform links the mechanism of plaque deposition in Alzheimer's disease

Yong Ming Li, Dennis W. Dickson

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

Alzheimer's disease (AD) brains contain high levels of advanced glycation endproducts (AGEs). Double immunostaining using anti-AGE and anti-apolipoprotein E (apoE) antibodies demonstrated that AGEs co-localized to a very high degree with apoE. We examined the binding of apoE to in vitro-prepared AGE-bovine serum albumin (AGE-BSA), using Western ligand blot analysis. ApoE exhibited AGE-specific binding activity in the presence of excess native BSA, with the dimeric form of apoE binding better than the monomeric form. Other apolipoproteins including apo A1, B, CI and CII, and serum β2-microglobulin, did not bind AGE-BSA. ApoE4 exhibited a 3-fold greater AGE-binding activity than the apoE3 isoform. These results suggest that apoE may participate in aggregate formation in the AD brain by binding to AGE-modified plaque components. It is possible that enhanced binding of apoE4 might have pathogenic consequences in vivo.

Original languageEnglish (US)
Pages (from-to)155-158
Number of pages4
JournalNeuroscience Letters
Volume226
Issue number3
DOIs
StatePublished - May 2 1997

Keywords

  • Alzheimer's disease
  • advanced glycation endproducts
  • apolipoprotein E

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Enhanced binding of advanced glycation endproducts (AGE) by the ApoE4 isoform links the mechanism of plaque deposition in Alzheimer's disease'. Together they form a unique fingerprint.

Cite this