一种NSAIDs的子集可以独立于循环氧基因酶活性来降低氨基胺基的Abeta42

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Preparation and In Vivo Use of an Activity-based Probe for N-acylethanolamine Acid Amidase
11:01

Preparation and In Vivo Use of an Activity-based Probe for N-acylethanolamine Acid Amidase

Published on: November 23, 2016

S Weggen1, J L Eriksen, P Das

  • 1Department of Neurosciences, University of California San Diego, La Jolla, California 92093, USA.

Nature
|November 9, 2001
PubMed
概括

非类固醇抗炎药物 (NSAIDs) 显著降低粉样β 42 (Abeta42) 水平,这是阿尔茨海默病的关键因素. 这种Abeta42降低发生在循环氧化酶抑制的独立性,这表明一种新的治疗途径.

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