In this article, we have discussed some of the latest and most important information from literature concerning the interactions of advanced glycation end products (AGEs), reactive oxygen species (ROS), NO-synthase and, especially, heme oxygenase (HO) in relation to the pathogenesis of Alzheimer's disease (AD). In addition, a new hypothesis of the possible pathomechanism in AD is presented. On the basis of the results from clinical and experimental studies, the role of dynamic changes in activity of NO and later CO producing reactions is postulated to play a crucial role in the development of AD at subcellular and molecular level. This theoretical assumption should be further proved by experimental research.
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