Abstract
The complex nature and genesis of oxidative damage in Alzheimer disease can be partly answered by mitochondrial and redox-active metal abnormalities. By releasing high levels of hydrogen peroxide, dysfunctional mitochondria propagate a series of interactions between redox-active metals and oxidative response elements. In the initial phase of disease development, amyloid-β deposition and hyperphosphorylated t may function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative injuries. However, during the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant activity representing a typical gain-offunction transformation, which can result from an increase in reactive species and a decrease in clearance mechanisms.
Keywords: alzheimer disease, amyloid-b, metal, mitochondria, oxidative stress
Current Alzheimer Research
Title: Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology
Volume: 2 Issue: 4
Author(s): Paula I. Moreira, Kazuhiro Honda, Quan Liu, Maria S. Santos, Catarina R. Oliveira, Gjumrakch Aliev, Akihiko Nunomura, Xiongwei Zhu, Mark A. Smith and George Perry
Affiliation:
Keywords: alzheimer disease, amyloid-b, metal, mitochondria, oxidative stress
Abstract: The complex nature and genesis of oxidative damage in Alzheimer disease can be partly answered by mitochondrial and redox-active metal abnormalities. By releasing high levels of hydrogen peroxide, dysfunctional mitochondria propagate a series of interactions between redox-active metals and oxidative response elements. In the initial phase of disease development, amyloid-β deposition and hyperphosphorylated t may function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative injuries. However, during the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant activity representing a typical gain-offunction transformation, which can result from an increase in reactive species and a decrease in clearance mechanisms.
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Cite this article as:
Moreira I. Paula, Honda Kazuhiro, Liu Quan, Santos S. Maria, Oliveira R. Catarina, Aliev Gjumrakch, Nunomura Akihiko, Zhu Xiongwei, Smith A. Mark and Perry George, Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology, Current Alzheimer Research 2005; 2 (4) . https://dx.doi.org/10.2174/156720505774330537
DOI https://dx.doi.org/10.2174/156720505774330537 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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