Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease

被引：87

作者：

Quinn, J

Montine, T

Morrow, J

Woodward, WR

Kulhanek, D

Eckenstein, F

机构：

[1] Portland Vet Affairs Med Ctr, Portland, OR 97201 USA

[2] Oregon Hlth Sci Univ, Dept Neurol, Portland, OR 97201 USA

[3] Univ Washington, Med Ctr, Dept Pathol, Seattle, WA 98195 USA

[4] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA

[5] Univ Vermont, Med Ctr, Dept Neurol, Burlington, VT USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2003年 / 137卷 / 1-2期

关键词：

Alzheimer; animal model; cyclooxygenase; nonsteroidal anti-inflammatory drug; oxidative stress; indomethacin; F2-isoprostanes;

D O I：

10.1016/S0165-5728(03)00037-7

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The hypothesis that inflammation and beta amyloid deposition are causally linked in Alzheimer's disease (AD) was tested in a transgenic mouse model. Untreated beta amyloid plaque-bearing Tg2576 mice did not differ from wild type animals in brain levels of most inflammatory mediators. Indomethacin treatment suppressed brain levels of prostaglandins by 90%, but reduced hippocampal beta amyloid by only 20%, with no effect on cortical beta amyloid. The discordant effects on beta amyloid and cyclooxygenase (COX) suggest that these effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are not causally linked. Further evidence against a causal relationship is seen in an unexpected trend to lower levels of beta amyloid after an inflammatory stimulus [lipopolysaccharide (LPS)]. (C) 2003 Elsevier Science B.V. All rights reserved.

引用

页码：32 / 41

页数：10

共 46 条

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