Oxidative posttranslational modifications in Alzheimer disease. A possible pathogenic role in the formation of senile plaques and neurofibrillary tangles.
The distinctive pathological lesions of Alzheimer disease (AD), senile plaques, and neurofibrillary tangles comprise aggregates of insoluble fibrillar protein. We and other investigators recently demonstrated that several mechanisms related to oxidative stress and free-radical reactions could play a crucial role in the pathogenesis of AD and, specifically, in the formation of senile plaques and neurofibrillary tangles (NFT).
Smith
M A
MA
Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Sayre
L M
LM
Monnier
V M
VM
Perry
G
G
D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000032:analysis; D006801:Humans; D008959:Models, Neurological; D016874:Neurofibrillary Tangles / Q000473:pathology*; D009474:Neurons / Q000473:pathology / Q000502:physiology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011499:Protein Processing, Post-Translational
D017127:Glycation End Products, Advanced