Kieseier B C, Storch M K, Hartung H P
Department of Neurology, Karl-Franzens-University, Graz, Austria.
J Neural Transm Suppl. 2000;59:69-80. doi: 10.1007/978-3-7091-6781-6_10.
A growing body of evidence supports the notion that inflammatory reactions in the central nervous system (CNS) are not only restricted to established immune mediated disorders, such as multiple sclerosis, but also contribute to the pathogenesis of Alzheimer's disease and other types of neurodegenerative disorders. The biological roles of toxic mediators, such as nitric oxide, reactive oxygen species, as well as complement and proteases in the genesis of inflammatory reactions in the CNS are reviewed within the context of demyelination and neuronal damage.
越来越多的证据支持这样一种观点,即中枢神经系统(CNS)中的炎症反应不仅局限于已确定的免疫介导疾病,如多发性硬化症,而且还促成了阿尔茨海默病和其他类型神经退行性疾病的发病机制。本文在脱髓鞘和神经元损伤的背景下,综述了一氧化氮、活性氧以及补体和蛋白酶等毒性介质在中枢神经系统炎症反应发生过程中的生物学作用。