Streit Wolfgang J
Department of Neuroscience, University of Florida College of Medicine Gainesville, FL, USA.
Front Aging Neurosci. 2010 Jun 3;2:22. doi: 10.3389/fnagi.2010.00022. eCollection 2010.
The neurofibrillary degeneration that occurs in Alzheimer's disease (AD) is thought to be the result of a chronic and damaging neuroinflammatory response mediated by neurotoxic substances produced by activated microglial cells. This neuroinflammation hypothesis of AD pathogenesis has led to numerous clinical trials with anti-inflammatory drugs, none of which have shown clear benefits for slowing or preventing disease onset and progression. In this paper, I make the point that AD is not an inflammatory condition, and reconstruct the sequence of events during the 1980s and 1990s that I believe led to the development of this faulty theory.
阿尔茨海默病（AD）中发生的神经纤维变性被认为是由活化的小胶质细胞产生的神经毒性物质介导的慢性损伤性神经炎症反应的结果。AD发病机制的这种神经炎症假说引发了众多使用抗炎药物的临床试验，但没有一项试验显示出在减缓或预防疾病发作及进展方面有明显益处。在本文中，我提出AD并非炎症性疾病，并重构了我认为导致这一错误理论在20世纪80年代和90年代发展的一系列事件。
