ABSTRACT
Alzheimer’s disease (AD) is a multifaceted neurodegenerative disease that, in most instances, does not have a clear cause. Numerous studies have examined the cellular, biochemical, and molecular changes that occur as a result of AD pathology. Oxidative stress and the excessive formation of chemically reactive species can be one of the pathways that link the biochemical changes and cellular dysfunction observed in AD.1,2 The elevated formation of chemically reactive species including lipid-derived carbonyls, peroxynitrite, and advanced glycation endproducts is well documented in AD.3-12 A wealth of data has been collected concerning the biochemical, neurotoxic, and cell signaling aspects of lipid-derived
carbonyls. These studies have been reviewed elsewhere.8,9,12-14 In this chapter, the formation and metabolism of lipid-derived carbonyls will be discussed.
