Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 62, Issue 5, Pages 486-496Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/jnen/62.5.486
Keywords
acetaldehyde; acetaldehyde-derived advanced glycation end products (AA-AGES); advanced glycation end products (AGES); alcoholism; neurotoxicity
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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.
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