Brain prolyl oligopeptidase activity is associated with neuronal damage rather than β-amyloid accumulation

被引：29

作者：

Laitinen, KSM

van Groen, T

Tanila, H

Venäläinen, J

Männistö, PT

Alafuzoff, I

机构：

[1] Univ Kuopio, Dept Pharmacol & Toxicol, FIN-70211 Kuopio, Finland

[2] Univ Kuopio, Dept Neurol & Neurosci, FIN-70211 Kuopio, Finland

[3] Kuopio Univ Hosp, Dept Pathol, SF-70210 Kuopio, Finland

来源：

NEUROREPORT | 2001年 / 12卷 / 15期

关键词：

Alzheimer's disease; beta-amyloid; neurofibrillary degeneration; prolyl oligopeptidase; transgenic mice;

D O I：

10.1097/00001756-200110290-00032

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Prolyl oligopeptidase (POP) have been suggested to participate in the pathogenesis of Alzheimer's disease (AD). In this study the activity of POP is evaluated in AD patients and in transgenic mice with substantial deposits of beta -amyloid (A beta). In AD cases, the POP activity displayed a significant negative correlation with the scores of senile/neuritic plaques and neurofibrillary tangles but not with A beta -load. The transgenic mice with high levels of A beta did not have altered POP activity compared to wild type mice. Based on our results, the low POP activity in AD seems to be associated with neuronal degeneration rather than to A beta accumulation. NeuroReport 12:3309-3312 (C) 2001 Lippincott Williams & Wilkins.

引用

页码：3309 / 3312

页数：4

共 20 条

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