TNFα plus IFNγ induce the production of Alzheimer β-amyloid peptides and decrease the secretion of APPs

被引：247

作者：

Blasko, I

Marx, F

Steiner, E

Hartmann, T

Grubeck-Loebenstein, B

机构：

[1] Austrian Acad Sci, Inst Biomed Aging Res, A-6020 Innsbruck, Austria

[2] Heidelberg Univ, Ctr Mol Biol Heidelberg, ZMBH, Heidelberg, Germany

来源：

FASEB JOURNAL | 1999年 / 13卷 / 01期

关键词：

tumor necrosis factor alpha; interferon gamma; beta APP; amyloid beta; Alzheimer's disease; glycosylation;

D O I：

10.1096/fasebj.13.1.63

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：

The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD), Multiple epidemiological studies also suggest that patients taking anti-inflammatory drugs have a decreased risk of developing AD. Here we present evidence that inflammatory cytokines can alter the metabolism of the beta-amyloid precursor protein (beta APP), We show that the combination of tumor necrosis factor alpha and interferon gamma triggers the production of beta-amyloid peptides and inhibits the secretion of soluble APPs by human neuronal and extraneuronal cells. The results demonstrate a new mechanism by which inflammatory components can exacerbate the fundamental pathology in AD.

引用

收藏

页码：63 / 68

页数：6

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