Abstract
β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimers disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.
Keywords: alzheimers disease, reactive oxygen species, hydrogen peroxide, superoxide, nitric oxide
Protein & Peptide Letters
Title: Induction of Cellular Oxidative Stress by the β-amyloid Peptide Involved in Alzheimers disease
Volume: 11 Issue: 3
Author(s): Gillian L. Gibson, David Allsop and Brian M. Austen
Affiliation:
Keywords: alzheimers disease, reactive oxygen species, hydrogen peroxide, superoxide, nitric oxide
Abstract: β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimers disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.
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Cite this article as:
Gibson L. Gillian, Allsop David and Austen M. Brian, Induction of Cellular Oxidative Stress by the β-amyloid Peptide Involved in Alzheimers disease, Protein & Peptide Letters 2004; 11 (3) . https://dx.doi.org/10.2174/0929866043407101
DOI https://dx.doi.org/10.2174/0929866043407101 |
Print ISSN 0929-8665 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5305 |
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