Amyloid beta peptide, 4-hydroxynonenal and apoptosis.
Considerable evidence suggests a role for oxidative stress in the pathogenesis of neuron degeneration in several neurodegenerative disorders including Alzheimer's disease (AD). Although debated, increasing evidence suggests that oxidative stress/damage (amyloid beta peptide, iron/hydrogen peroxide) or neurotoxic by-products of lipid peroxidation (4-hydroxy-2-nonenal, acrolein) lead to cell death through apoptosis or programmed cell death in AD. This review discusses current evidence supporting the role of oxidative stress/damage mediated apoptosis in in vitro models of neurodegeneration.
Lovell
Mark A
MA
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA. malove2@uky.edu
Markesbery
William R
WR
D000447:Aldehydes / Q000378:metabolism* / Q000633:toxicity; D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D002478:Cells, Cultured / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology*
D000447:Aldehydes; D016229:Amyloid beta-Peptides; C027576:4-hydroxy-2-nonenal