环氧合酶在神经变性疾病神经元进行性损伤中起重要作用

环氧合酶(COX)是非甾体抗炎药的主要作用靶点.自从上世纪90年代初被发现至今,COX已被证实广泛参与炎性反应过程.小胶质细胞是介导"神经炎性反应"的主要细胞类型,过去十年中,COX通路参与小胶质细胞激活及神经变性过程的机制取得了很大进展.本文对该领域的新近研究成果予以论述,并以三大神经变性疾病,即阿尔采末病(AD)、帕金森病(PD)和肌萎缩侧索硬化症(ALS)为例,对COX在其发病中的作用加以阐释,突出该领域的研究热点,为神经变性疾病发病机制及药物治疗研究提供新的思路.

COX plays a pivotal role in the progressive neuronal loss in neurodegenerative diseases

Cyclooxygenase (COX) is the major target of non-steroidal anti-inflammatory drugs (NSAIDs). Since its discovery in the early 1990s, COX has been identified as a major player in inflammatory reactions. "neuroinflammation" is triggered and sustained by activation of resident cells, particularly microglia. Intensive researches have been made in the last decade concerning the COX pathway and its effect on microglial activation as well as other processes involved in neurondegeneration. This article reviewed new data in this area, focusing on three major neurodegenerative diseases, Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). By highlighting current knowledge in this field, it may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.