Abstract
Oxidative stress in brain is emerging as a potential causal factor in aging and age-related neurodegenerative disorders. Brain tissue from living patients is difficult to acquire; hence, animal models of aging and age-related neurodegenerative disorders, though not perfect models, have provided tissue to study the role of oxidative stress in these disorders. In this review, the central role of oxidative damage in brain in models of accelerated aging (progeria and Werners syndrome) and the age-related neurodegenerative disorders, Alzheimers disease and Huntingtons disease, will be presented and evaluated. To the extent that the animal models faithfully mirror their respective disorders, and based on the totality of the studies, it is apparent that oxidative stress, the excess of free radicals over the means of scavenging these harmful agents, may play critical roles in the molecular basis of accelerated aging, Alzheimers disease, and Huntingtons disease.
Keywords: Neurodegenerative Disorders, Alzheimers Disease, Huntingtons Disease, Oxidative Stress in
Current Medicinal Chemistry
Title: Brain Oxidative Stress in Animal Models of Accelerated Aging and the Age-related Neurodegenerative Disorders, Alzheimers Disease and Huntingtons Disease
Volume: 8 Issue: 7
Author(s): D. Allan Butterfield, Beverly J. Howard and Michael A. LaFontaine
Affiliation:
Keywords: Neurodegenerative Disorders, Alzheimers Disease, Huntingtons Disease, Oxidative Stress in
Abstract: Oxidative stress in brain is emerging as a potential causal factor in aging and age-related neurodegenerative disorders. Brain tissue from living patients is difficult to acquire; hence, animal models of aging and age-related neurodegenerative disorders, though not perfect models, have provided tissue to study the role of oxidative stress in these disorders. In this review, the central role of oxidative damage in brain in models of accelerated aging (progeria and Werners syndrome) and the age-related neurodegenerative disorders, Alzheimers disease and Huntingtons disease, will be presented and evaluated. To the extent that the animal models faithfully mirror their respective disorders, and based on the totality of the studies, it is apparent that oxidative stress, the excess of free radicals over the means of scavenging these harmful agents, may play critical roles in the molecular basis of accelerated aging, Alzheimers disease, and Huntingtons disease.
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Cite this article as:
Butterfield Allan D., Howard J. Beverly and LaFontaine A. Michael, Brain Oxidative Stress in Animal Models of Accelerated Aging and the Age-related Neurodegenerative Disorders, Alzheimers Disease and Huntingtons Disease, Current Medicinal Chemistry 2001; 8 (7) . https://dx.doi.org/10.2174/0929867013373048
DOI https://dx.doi.org/10.2174/0929867013373048 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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