title: Hydroxynonenal, toxic carbonyls, and Alzheimer disease.
abstract: Cytoskeletal disruption is one of the distinguishing characteristics of the vulnerable neurons in Alzheimer disease (AD). It has been suggested that these cytoskeletal changes occur secondarily to covalent modifications of the protein components. Despite the abundance and probable importance of these changes, there has been very little data regarding the identity of the modified proteins or the precise chemistry of the modifications. Here we review a specific type of modification, namely carbonylation of proteins, which has been shown to be a common result of cellular oxidative stress. Hopefully, the following discussion will help elucidate the relationship between oxidative stress, protein modification and the pathogenesis of AD.
authors.affiliation: Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA.
authors.forename: Quan
authors.initials: Q
authors.lastname: Liu
authors.forename: Arun K
authors.initials: AK
authors.lastname: Raina
authors.forename: Mark A
authors.initials: MA
authors.lastname: Smith
authors.forename: Lawrence M
authors.initials: LM
authors.lastname: Sayre
authors.forename: George
authors.initials: G
authors.lastname: Perry
mesh_terms: D000447:Aldehydes / Q000378:metabolism*; D000544:Alzheimer Disease / Q000378:metabolism*; D000818:Animals; D001369:Axons / Q000378:metabolism; D006801:Humans; D016900:Neurofilament Proteins / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*
chemical_list: D000447:Aldehydes; D016900:Neurofilament Proteins; C027576:4-hydroxy-2-nonenal