Thomas T, Nadackal T G, Thomas K
Woodlands Medical Center and Endron Therapeutics, 3150 Tampa Road, #16 Oldsmar, FL 34677, USA.
Neuroreport. 2001 Oct 29;12(15):3263-7. doi: 10.1097/00001756-200110290-00024.
The neurotoxic and proinflammatory actions of the Alzheimer peptide amyloid-beta (Abeta) are dependent on its aggregation and beta-sheet conformation. Chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin for arthritis decreases the risk of developing Alzheimer's disease (AD) by unknown mechanisms. We report that these drugs inhibit human Abeta aggregation in vitro and reverse the beta-sheet conformation of preformed fibrils at clinically relevant doses. Aspirin prevented enhanced Abeta aggregation by aluminum, an environmental risk factor for AD. This anti-aggregatory effect was restricted to NSAIDs and was not exhibited by other drugs used in AD therapy. NSAIDS may have a role in the prevention and treatment of AD, in addition to a number of age-related disorders such as arthritis, cardiovascular disease and cancer.
阿尔茨海默病肽β-淀粉样蛋白（Aβ）的神经毒性和促炎作用取决于其聚集和β-折叠构象。长期使用阿司匹林等非甾体抗炎药（NSAIDs）治疗关节炎可通过未知机制降低患阿尔茨海默病（AD）的风险。我们报告称，这些药物在体外可抑制人Aβ聚集，并在临床相关剂量下逆转预先形成的纤维的β-折叠构象。阿司匹林可预防铝增强的Aβ聚集，铝是AD的一个环境风险因素。这种抗聚集作用仅限于NSAIDs，而AD治疗中使用的其他药物则不具有此作用。除了关节炎、心血管疾病和癌症等一些与年龄相关的疾病外，NSAIDs可能在AD的预防和治疗中发挥作用。
