alpha-1-Antichymotrypsin interaction with A beta (1-40) inhibits fibril formation but does not affect the peptide toxicity

被引：36

作者：

Aksenova, MV

Aksenov, MY

Butterfield, DA

Carney, JM

机构：

[1] UNIV KENTUCKY,DEPT CHEM,LEXINGTON,KY 40506

[2] UNIV KENTUCKY,CTR MEMBRANE SCI,LEXINGTON,KY 40506

来源：

NEUROSCIENCE LETTERS | 1996年 / 211卷 / 01期

关键词：

amyloid; alpha-1-antichymotrypsin; neurotoxicity; fibril formation;

D O I：

10.1016/0304-3940(96)12717-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Recent studies have shown that senile plaque-associated or glial-derived proteins can prevent fibril formation of beta-amyloid peptide (A beta), while increasing the neurotoxicity of the latter (in the case of glutamine synthetase, apolipoprotein J or thrombin). alpha-1-Antichymotrypsin (ACT) is a glial-derived protein associated with senile plaques in the Alzheimer's brain. In this report we show that ACT, a minor protein component of beta-amyloid deposits, is able to inhibit A beta (1-40) aggregation into fibrils, but unable to modulate the toxicity of A beta (1-40) in primary rat hippocampal cell cultures. These results are discussed in terms of the potential role of glial-derived proteins on A beta aggregation and neurotoxicity.

引用

收藏

页码：45 / 48

页数：4

相关论文

共 21 条

[1]

IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE [J].

ABRAHAM, CR ;

SELKOE, DJ ;

POTTER, H .

CELL, 1988, 52 (04) :487-501

[2]

Aksenov MY, 1996, J NEUROCHEM, V66, P2050

[3]

BETA-AMYLOID PEPTIDE FREE-RADICAL FRAGMENTS INITIATE SYNAPTOSOMAL LIPOPEROXIDATION IN A SEQUENCE-SPECIFIC FASHION - IMPLICATIONS TO ALZHEIMERS-DISEASE [J].

BUTTERFIELD, DA ;

HENSLEY, K ;

HARRIS, M ;

MATTSON, M ;

CARNEY, J .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 200 (02) :710-715

[4]

FIBRILLOGENESIS IN ALZHEIMERS-DISEASE OF AMYLOID-BETA PEPTIDES AND APOLIPOPROTEIN-E [J].

CASTANO, EM ;

PRELLI, F ;

WISNIEWSKI, T ;

GOLABEK, A ;

KUMAR, RA ;

SOTO, C ;

FRANGIONE, B .

BIOCHEMICAL JOURNAL, 1995, 306 :599-604

[5]

ALPHA(1)-ANTICHYMOTRYPSIN REGULATES ALZHEIMER BETA-AMYLOID PEPTIDE FIBRIL FORMATION [J].

ERIKSSON, S ;

JANCIAUSKIENE, S ;

LANNFELT, L .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (06) :2313-2317

[6]

ALPHA-1-ANTICHYMOTRYPSIN BINDING TO ALZHEIMER A-BETA PEPTIDES IS SEQUENCE-SPECIFIC AND INDUCES FIBRIL DISAGGREGATION INVITRO [J].

FRASER, PE ;

NGUYEN, JT ;

MCLACHLAN, DR ;

ABRAHAM, CR ;

KIRSCHNER, DA .

JOURNAL OF NEUROCHEMISTRY, 1993, 61 (01) :298-305

[7]

A MODEL FOR BETA-AMYLOID AGGREGATION AND NEUROTOXICITY BASED ON FREE-RADICAL GENERATION BY THE PEPTIDE - RELEVANCE TO ALZHEIMER-DISEASE [J].

HENSLEY, K ;

CARNEY, JM ;

MATTSON, MP ;

AKSENOVA, M ;

HARRIS, M ;

WU, JF ;

FLOYD, RA ;

BUTTERFIELD, DA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (08) :3270-3274

[8]

CROSS-LINKING OF A SYNTHETIC PARTIAL-LENGTH (1-28) PEPTIDE OF THE ALZHEIMER BETA/A4 AMYLOID PROTEIN BY TRANSGLUTAMINASE [J].

IKURA, K ;

TAKAHATA, K ;

SASAKI, R .

FEBS LETTERS, 1993, 326 (1-3) :109-111

[9]

EFFECT OF ALPHA(1)-ANTICHYMOTRYPSIN ON THE TOXICITY OF BETA-AMYLOID FRAGMENT-25-40 IN RAT PRIMARY CULTURED NEURONS [J].

KOBAYASHI, T ;

ABE, K ;

SAITO, H ;

NISHIYAMA, N .

NEUROSCIENCE LETTERS, 1994, 172 (1-2) :147-150

[10]

BETA-AMYLOID NEUROTOXICITY REQUIRES FIBRIL FORMATION AND IS INHIBITED BY CONGO RED [J].

LORENZO, A ;

YANKNER, BA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :12243-12247