Rogers J
L. J. Roberts Center, Sun Health Research Institute, Sun City, Arizona, USA.
Arzneimittelforschung. 1995 Mar;45(3A):439-42.
Numerous markers of inflammation have been reported in the Alzheimer's disease brain. Although other pathogenic mechanisms certainly apply, there is now compelling evidence that inflammation is not simply a response to already existing Alzheimer's pathology, but ultimately becomes a significant source of pathology. The pathogenic potential of inflammation in Alzheimer's disease follows from the inherent destructiveness of inflammatory mechanisms, the postmitotic status of neurons, and the unique interactions of inflammatory markers and cells with pathologic hallmarks of Alzheimer's such as amyloid beta-peptide. These conclusions from basic science are borne out by recent clinical efforts, though the latter are still limited and require further confirmation.
在阿尔茨海默病大脑中已报道了众多炎症标志物。尽管其他致病机制肯定也起作用，但现在有令人信服的证据表明，炎症并非仅仅是对已存在的阿尔茨海默病病理学的一种反应，而是最终成为病理学的一个重要来源。阿尔茨海默病中炎症的致病潜力源于炎症机制的内在破坏性、神经元的终末有丝分裂状态，以及炎症标志物和细胞与阿尔茨海默病病理特征（如β-淀粉样肽）的独特相互作用。基础科学得出的这些结论得到了近期临床研究的证实，尽管后者仍然有限且需要进一步确认。
