Inflammation and Alzheimer's disease pathogenesis
Inflammation and Alzheimer's disease pathogenesis
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DOI：
10.1016/0197-4580(96)00115-7
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发表时间：
1996-09-01
影响因子：
4.2
通讯作者：
McGeer, P
中科院分区：
文献类型：
--
作者：
Rogers, J;Webster, S;McGeer, P
对炎症介质在阿尔茨海默病 (AD) 发病机制中所起作用的认识仍然受到两个相关误解的阻碍。首先，要具有重要的致病机制，神经退行性机制必须是主要的。第二个是炎症的发生只是为了清除已经存在的病理碎屑。本综述通过表明 1) 炎症分子和机制在 AD 大脑中独特存在或显着升高，2) 炎症可能是 AD 发病机制的必要组成部分，3) 炎症可能足以引起 AD 神经变性，4) 回顾性和直接临床试验表明，传统抗炎药物在减缓 AD 进展甚至延缓 AD 发病方面具有治疗益处。
Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existant pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenesis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD.