Influence of heparin and dendrimers on the aggregation of two amyloid peptides related to Alzheimer's and prion diseases

被引：103

作者：

Klajnert, B

Cortijo-Arellano, M

Bryszewska, M

Cladera, J ^{[1
]}

机构：

[1] Univ Autonoma Barcelona, Fac Med, Biophys Unit, Dept Biochem & Mol Biol, Bellaterra 08193, Catalonia, Spain

[2] Univ Lodz, Dept Gen Biophys, PL-90237 Lodz, Poland

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 339卷 / 02期

关键词：

amyloid; Alzheimer; prion; dendrimer; heparin;

D O I：

10.1016/j.bbrc.2005.11.053

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：

Amyloid plaques composed of proteinaceous aggregates are commonly found in brains affected by Alzheimer's disease and spongiform encephalopaties. A structural homology has been recently described for the Alzheimer's peptide A beta 1-28 and the segment of the prion protein Prp185-208. In the present paper, further elements in common are reported: the aggregation processes are in both cases enhanced by the model glucosaminoglycan heparin and dendrimers can modulate the aggregation process by affecting the nucleation rate at low concentrations and the elongation rate at high concentrations. Nucleation and elongation rate constants are derived from fittings to a nucleation dependent polymerization model. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：577 / 582

页数：6