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Metabolic, Metallic and Mitotic Sources of Oxidative Stress in Alzheimer Disease
Smith, Mark A.,Zhu, Xiongwei,Nunomura, Akihiko,Raina, Arun K.,Rottkamp, Catherine A.,Takeda, Atsushi,Perry, George 한림대학교 환경·생명과학연구소 2000 국제학술회의 Vol.2000 No.-
Alzheimer disease(AD) is marked by increases in oxidative damage to macromolecules such as sugars, lipids, proteins and nucleic acids. Notably, such damage is not limited to the lesions of the disease but instead involves all vulnerable neurons. These findings of oxidative abnormalities clearly predate gross described neuronal cytopathology and support the primacy of oxidative damage as an early and dynamic change of AD. Here, we review possible sources of oxidative damage as it applies to AD. Contrary to in vitro findings, correlations between cases with various extents of amyloid-β deposits or neurofibrillary tangles(NFT) show that oxidative damage is in fact reduced with increasing senile plaque and neurofibrillary tangle density (Nunomura et at., 1999a). For amyloid-β, there is a direct negative linear correlation with oxidative damage (Nunomura et at., 1999b). These findings indicate that the formation of the amyloid-β plaques and NFT, long thought of as a deleterious process leading to neuronal death, may in fact be a cytoprotective response(Morsch et at., 1999) to reduce oxidative damage.
Metabolic, Metallic and Mitotic Sources of Oxidative Stress in Alzheimer Disease
Smith, Mark A.,Zhu, Xiongwei,Nunomura, Akihiko,Raina, Arun K.,Rottkamp, Catherine A.,Takeda , Atsushi,Perry, George 한림대학교 환경·생명과학연구소 2000 [일송 국제심포지엄] 노화와 만성퇴행성 신경질환 Vol.- No.3
Alzheimer disease (AD) is marked by increases in oxidative damage to macromolecules such as sugars, lipids, proteins and nucleic acids. Notably, such damage is not limited to the lesions of the disease but instead involves all vulnerable neurons. These findings of oxidative abnormalities clearly predate gross described neuronal cytopathology and support the primacy of oxidative damage as an early and dynamic change of AD. Here, we review possible sources of oxidative damage as it applies to AD. Contrary to in vitro findings, correlations between cases with various extents of amyloid-β deposits or neurofibrillary tangles (NFT) show that oxidative damage is in fact reduced with increasing senile plaque and neurofibrillary tangle density (Nunomura et al., 1999a). for amyloid-β, there is a direct negative linear correlation with oxidative damage (Nunomura et al., 1999b). These findings indicate that the formation of the amyloid-β plaques and NFT, long thought of as a deleterious process leading to neuronal death, may in fact be a cytoprotective response (Morsch et al.,1999) to reduce oxidative damage.