Abstract
Although iron is essential in maintaining the function of the central nervous system, it is a source of reactive oxygen species, which is potentially neurotoxic. Excess iron accumulation has been reported to be associated with many neurodegenerative diseases including Alzheimer disease. Because oxidative damage to neurons is suggested to be an early event of Alzheimer disease, iron deposition in the central nervous system may play a pivotal role in its pathogenesis. In fact, in Alzheimer disease, iron has been demonstrated histochemically to be present in senile plaques and neurofibrillary tangles, the main constituents being amyloid-β and tau, respectively. Since these molecules are key in the pathogenesis of Alzheimer disease, many studies have focused on the relationship of iron with them. However, it has been shown that the oxidative change in neurons is observed before the formation of these pathological hallmarks. This review discusses the suggested role of iron in the progression of Alzheimer disease.
Keywords: alzheimer disease, chelation, neurodegeneration, oxidative stress, redox active iron
Letters in Drug Design & Discovery
Title: Redox Active Iron at the Center of Oxidative Stress in Alzheimer Disease
Volume: 2 Issue: 6
Author(s): Kazuhiro Honda, Paula I. Moreira, Quan Liu, Sandra L. Siedlak, Xiongwei Zhu, Mark A Smith and George Perry
Affiliation:
Keywords: alzheimer disease, chelation, neurodegeneration, oxidative stress, redox active iron
Abstract: Although iron is essential in maintaining the function of the central nervous system, it is a source of reactive oxygen species, which is potentially neurotoxic. Excess iron accumulation has been reported to be associated with many neurodegenerative diseases including Alzheimer disease. Because oxidative damage to neurons is suggested to be an early event of Alzheimer disease, iron deposition in the central nervous system may play a pivotal role in its pathogenesis. In fact, in Alzheimer disease, iron has been demonstrated histochemically to be present in senile plaques and neurofibrillary tangles, the main constituents being amyloid-β and tau, respectively. Since these molecules are key in the pathogenesis of Alzheimer disease, many studies have focused on the relationship of iron with them. However, it has been shown that the oxidative change in neurons is observed before the formation of these pathological hallmarks. This review discusses the suggested role of iron in the progression of Alzheimer disease.
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Cite this article as:
Honda Kazuhiro, Moreira I. Paula, Liu Quan, Siedlak L. Sandra, Zhu Xiongwei, Smith A Mark and Perry George, Redox Active Iron at the Center of Oxidative Stress in Alzheimer Disease, Letters in Drug Design & Discovery 2005; 2 (6) . https://dx.doi.org/10.2174/1570180054771545
DOI https://dx.doi.org/10.2174/1570180054771545 |
Print ISSN 1570-1808 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-628X |
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