| Literature DB >> 12769188 |
Masayoshi Takeuchi1, Takayuki Watai, Nobuyuki Sasaki, Hiroshi Choei, Mina Iwaki, Takeshi Ashizawa, Yosuke Inagaki, Sho-Ichi Yamagishi, Seiji Kikuchi, Peter Riederer, Toshikazu Saito, Richard Bucala, Yukihiko Kameda.
Abstract
The Maillard reaction that leads to the formation of advanced glycation end products (AGEs) plays an important role in the pathogenesis of angiopathy in diabetic patients, in aging, and in neurodegenerative processes. We hypothesize that acetaldehyde (AA), one of the main metabolites of alcohol, may be involved in alcohol-induced neurotoxicity in vivo by formation of AA-derived AGEs (AA-AGEs) with brain proteins. Incubation of cortical neurons with AA-AGE produced a dose-dependent increase in neuronal cell-death, and the neurotoxicity of AA-AGE was neutralized by the addition of an anti-AA-AGE-specific antibody, but not by anti-N-ethyllysine (NEL) antibody. The AA-AGE epitope was detected in human brain of alcoholism. We propose that the structural epitope AA-AGE is an important toxic moiety for neuronal cells in alcoholism.Entities:
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Year: 2003 PMID： 12769188 DOI： 10.1093/jnen/62.5.486
Source DB: PubMed Journal: J Neuropathol Exp Neurol ISSN： 0022-3069 Impact factor: 3.685