ATTENUATION OF THE NEUROTOXIC EFFECT OF A-BETA AMYLOID PEPTIDE BY APOLIPOPROTEIN-E

被引：67

作者：

WHITSON, JS

MIMS, MP

STRITTMATTER, WJ

YAMAKI, T

MORRISETT, JD

APPEL, SH

机构：

[1] BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030

[2] BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030

[3] DUKE UNIV,MED CTR,DEPT MED NEUROL & NEUROBIOL,DURHAM,NC 27710

[4] KYOTO PREFECTURAL UNIV MED,DEPT NEUROSURG,KAMIGYO KU,KYOTO 602,JAPAN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1994年 / 199卷 / 01期

关键词：

D O I：

10.1006/bbrc.1994.1209

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alzheimer's disease patients have increased frequency of apolipoprotein E allele c4, suggesting apoE4 is a risk factor determining disease. ApoE binds A beta amyloid peptide with great avidity in vitro and in the neuritic plaque. Potentially, binding of A beta to apolipoprotein E could increase A beta neurotoxicity. However, in hippocampal cultures, 0.1 mu M apolipoprotein E eliminated the neurotoxicity of 10 mu M A beta. Neuronal rescue was dose-dependent and occurred even after 48 hours exposure to A beta, but was overwhelmed by excess A beta. Thus, interaction between these proteins does not directly increase A beta neurotoxicity, and the role of ApoE in Alzheimer's disease remains to be elucidated. (C) 1994 Academic Press, Inc.

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页码：163 / 170

页数：8

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