Zamani M R, Allen Y S, Owen G P, Gray J A
Department of Human Anatomy and Cell Biology, University of Liverpool, UK.
Neuroreport. 1997 Jan 20;8(2):513-7. doi: 10.1097/00001756-199701200-00027.
Two major features of Alzheimer's disease (AD) are beta-amyloid protein (beta AP) deposition and a severe cholinergic deficit. An association between the two is suggested by the negative correlation found between cigarette smoking and AD. We sought to investigate this further by examining the effects of acute and chronic nicotine exposure on beta AP-induced neuronal loss in rat hippocampal cultures. Nicotine was found to attenuate the neurotoxicity of higher concentrations of beta AP(25-35), an effect which was enhanced by longer nicotine pretreatment and significantly inhibited by the nicotine receptor antagonist mecamylamine. Our results suggest that nicotine partially protects against the neurotoxic actions of beta AP(25-35) via a receptor-mediated pathway.
阿尔茨海默病（AD）的两个主要特征是β-淀粉样蛋白（βAP）沉积和严重的胆碱能缺陷。吸烟与AD之间的负相关表明了两者之间的关联。我们试图通过研究急性和慢性尼古丁暴露对大鼠海马体培养物中βAP诱导的神经元损失的影响来进一步探究这一关联。研究发现，尼古丁可减弱较高浓度βAP（25 - 35）的神经毒性，延长尼古丁预处理可增强这一效果，而尼古丁受体拮抗剂美加明则可显著抑制该效果。我们的结果表明，尼古丁通过受体介导的途径部分保护神经元免受βAP（25 - 35）的神经毒性作用。
