title: Effect of advanced glycation endproducts on cell cycle and their relevance for Alzheimer's disease.
abstract: In Alzheimer's disease, neurons in affected regions re-enter the cell cycle, leave the G0 state and appear to be arrested at both the G1/S and G2/M phase with resulting cell death, predominantly by apoptosis. Further hallmarks of AD are crosslinked protein deposits (amyloid plaques and neurofibrillary tangles), which time-dependently become modified by "advanced glycation endproducts (AGEs)". Since AGEs activate both mitogenic and redox-sensitive pathways, they might be involved both in cell cycle re-entry and arrest.
authors.affiliation: Neuroimmunological Cell Biology Unit, IZKF Leipzig, Germany. mueg@medizin.uni-leipzig.de
authors.forename: G
authors.initials: G
authors.lastname: Münch
authors.forename: J
authors.initials: J
authors.lastname: Gasic-Milenkovic
authors.forename: T
authors.initials: T
authors.lastname: Arendt
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D002453:Cell Cycle; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction
chemical_list: D017127:Glycation End Products, Advanced