Human amyloid-β1-42 applied in vivo inhibits the fast axonal transport of proteins in the sciatic nerve of rat

被引：30
|
作者：
Kasa, P
Papp, H
Kovacs, I
Forgon, M
Penke, B
Yamaguchi, H
机构：
[1] Albert Szent Gyorgyi Med Univ, Alzheimers Dis Res Ctr, H-6720 Szeged, Hungary
[2] Albert Szent Gyorgyi Med Univ, Dept Med Chem, H-6720 Szeged, Hungary
[3] Gunma Univ, Coll Med Care & Technol, Maebashi, Gumma 371, Japan
来源：
NEUROSCIENCE LETTERS | 2000年 / 278卷 / 1-2期
基金：
匈牙利科学研究基金会;
关键词：
Alzheimer's disease; amyloid; axonal transport; immunohistochemistry; neurotoxicity; sciatic nerve;
D O I：
10.1016/S0304-3940(99)00863-0
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Human amyloid-beta 1-42 has been suggested to be a pathogenetic factor in Alzheimer's disease. The precise mechanism by which this peptide causes the degeneration of neurons in the affected brain is not yet fully understood. By using immunohistochemistry we explored the inhibitory effects of human amyloid-beta 1-42 applied in vivo on the fast axonal transport of acetylcholinesterase, the amyloid precursor protein, the vesicular acetylcholine transporter and synaptophysin in the sciatic nerve of rat. Our findings provide evidence for the in vivo neurotoxic effect of human amyloid-beta peptide. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码：117 / 119
页数：3
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