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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease.
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Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease.

机译：在阿尔茨海默氏病动物模型中，炎症和脑淀粉样变性病是不连续的。

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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)].
机译：在转基因小鼠模型中测试了在阿尔茨海默氏病（AD）中炎症和β淀粉样蛋白沉积有因果关系的假说。未经处理的带有β淀粉样蛋白斑块的Tg2576小鼠在大多数炎症介质的大脑水平上与野生型动物没有区别。消炎痛治疗可将脑内前列腺素水平降低90％，但将海马β淀粉样蛋白降低20％，而对皮质β淀粉样蛋白无影响。对β淀粉样蛋白和环氧合酶（COX）的不一致作用表明，非甾体抗炎药（NSAID）的这些作用没有因果关系。在因炎症刺激[脂多糖（LPS）]后，β-淀粉样蛋白水平降低的出乎意料的趋势中发现了进一步的因果关系证据。

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