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

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 beta2-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.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Li YM,Dickson DW

doi

10.1016/s0304-3940(97)00266-8

subject

Has Abstract

pub_date

1997-05-02 00:00:00

pages

155-8

issue

3

eissn

0304-3940

issn

1872-7972

pii

S0304394097002668

journal_volume

226

pub_type

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