Aisen Paul S
Department of Neurology, Georgetown University Medical Center, Washington DC 20007, USA.
Lancet Neurol. 2002 Sep;1(5):279-84. doi: 10.1016/s1474-4422(02)00133-3.
Genetic evidence suggests that generation of amyloid beta peptide is the pivotal step in the pathophysiology of Alzheimer's disease (AD). The mechanism by which this peptide induces neurodegeneration may involve inflammatory processes. Pharmacological suppression of inflammation may therefore ameliorate the neuropathology. Basic research studies provide substantial evidence that inflammatory processes present in the brains of patients with AD are destructive, and that anti-inflammatory drugs can provide protection. Furthermore, epidemiological studies suggest that anti-inflammatory drugs reduce the risk of AD. However, there is not yet any strong evidence from completed randomised controlled trials that anti-inflammatory treatment is beneficial. Large trials of glucocorticoid therapy, hydroxychloroquine, and non-steroidal anti-inflammatory drugs (NSAIDs) in the treatment of AD have so far been disappointing. Several studies, including a large primary prevention trial with NSAIDs, are still in progress. Major issues of selection of patients, drug regimen, and duration of treatment remain unresolved.
遗传学证据表明，β-淀粉样肽的产生是阿尔茨海默病（AD）病理生理学中的关键步骤。该肽诱导神经变性的机制可能涉及炎症过程。因此，药理学上抑制炎症可能会改善神经病理学。基础研究提供了大量证据，表明AD患者大脑中存在的炎症过程具有破坏性，且抗炎药物可以提供保护作用。此外，流行病学研究表明，抗炎药物可降低患AD的风险。然而，尚无来自已完成的随机对照试验的有力证据表明抗炎治疗有益。迄今为止，糖皮质激素疗法、羟氯喹和非甾体抗炎药（NSAIDs）治疗AD的大型试验结果令人失望。包括一项使用NSAIDs的大型一级预防试验在内的多项研究仍在进行中。患者选择、药物方案和治疗持续时间等主要问题仍未得到解决。
