COX-1和COX-2在阿尔茨海默病病理中的作用及非甾体抗炎药的治疗潜力

Jeroen J M Hoozemans, M Kerry O'Banion
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引用次数: 97

摘要

流行病学研究表明,抗炎药物,特别是非甾体抗炎药(NSAIDs),可以降低患阿尔茨海默病(AD)的风险。它们的有益作用可能是由于干扰了阿尔茨海默病的慢性炎症反应。非甾体抗炎药最典型的作用是抑制环氧化酶(COX)。到目前为止,旨在抑制炎症或环氧合酶活性的临床试验在治疗AD患者方面都失败了。本文就COX-1和COX-2在神经退行性疾病和AD发病中的作用、表达和调控作一综述。了解环加氧酶的病理、生理和神经保护作用将有助于开发治疗或预防AD的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of COX-1 and COX-2 in Alzheimer's disease pathology and the therapeutic potentials of non-steroidal anti-inflammatory drugs.

Epidemiological studies indicate that anti-inflammatory drugs, especially the non-steroidal anti-inflammatory drugs (NSAIDs), decrease the risk of developing Alzheimer's disease (AD). Their beneficial effects may be due to interference of the chronic inflammatory reaction in AD. The best-characterised action of NSAIDs is the inhibition of cyclooxygenase (COX). So far, clinical trials designed to inhibit inflammation or cyclooxygenase activity have failed in the treatment of AD patients. In this review we will focus on the role, expression and regulation of COX-1 and COX-2 in neurodegeneration and AD pathogenesis. Understanding the pathological, physiological and neuroprotective role of cyclooxygenase will contribute to the development of a therapy for the treatment or prevention of AD.

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