title: Advanced glycation endproducts as gerontotoxins and biomarkers for carbonyl-based degenerative processes in Alzheimer's disease.
abstract: Alzheimer's disease (AD) is the most common dementia disorder of later life. Although there might be various different triggering events in the early stages of the disease, they appear to converge on a few characteristic final pathways in the late stages, characterized by inflammation and neurodegeneration. Here, we review the hypothesis that advanced glycation end products (AGEs), which reflect carbonyl stress, an imbalance between the production of reactive carbonyl compounds and their detoxification, can serve as biomarkers for the progression of disorder. AGE modification may explain many of the neuropathological and biochemical features of AD, such as extensive protein cross-linking shown as amyloid plaques and neurofibrillary tangles, inflammation, oxidative stress and neuronal cell death. Although accumulation of AGEs is a normal feature of aging, it appears to be significantly accelerated in AD. We suggest that higher AGE concentrations in brain tissue and in cerebrospinal fluid might be able to distinguish between normal aging and AD.
authors.affiliation: Department of Pharmacology, School of Medicine, University of Western Sydney, Campbelltown, Australia.
authors.forename: Anton
authors.initials: A
authors.lastname: Rahmadi
authors.forename: Nicole
authors.initials: N
authors.lastname: Steiner
authors.forename: Gerald
authors.initials: G
authors.lastname: Münch
mesh_terms: D000544:Alzheimer Disease / Q000175:diagnosis / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000032:analysis / Q000378:metabolism*; D006801:Humans
chemical_list: D015415:Biomarkers; D017127:Glycation End Products, Advanced