Journal ArticleDOI
Oxidative stress in brain aging: Implications for therapeutics of neurodegenerative diseases
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TLDR
Novel therapeutics based on blocking neuron damaging neuroinflammatory processes show great promise for abating dementia progression although they have yet to make it to clinical practice and non-steroidal anti-inflammatory drugs show significant promise.About:
This article is published in Neurobiology of Aging.The article was published on 2002-09-01. It has received 792 citations till now. The article focuses on the topics: Aging brain & Alzheimer's disease.read more
Citations
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Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options.
TL;DR: Recognition of upstream and downstream antioxidant therapy to oxidative stress has been proved an effective tool in alteration of any neuronal damage as well as free radical scavenging.
Journal Article
Studies on free radicals, antioxidants, and co-factors.
TL;DR: The aim of this review is to highlight the main themes from studies on free radicals, antioxidants and co-factors, and to propose an evidence-based strategy for healthy aging.
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Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
Roy G. Cutler,Jeremiah F. Kelly,Kristin Storie,Ward A. Pedersen,Anita Tammara,Kimmo J. Hatanpaa,Juan C. Troncoso,Mark P. Mattson,Mark P. Mattson +8 more
TL;DR: These findings suggest a sequence of events in the pathogenesis of AD in which Aβ induces membrane-associated oxidative stress, resulting in perturbed ceramide and cholesterol metabolism which, in turn, triggers a neurodegenerative cascade that leads to clinical disease.
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Ageing and neuronal vulnerability
Mark P. Mattson,Tim Magnus +1 more
TL;DR: Emerging evidence on protein interaction networks that monitor and respond to the normal ageing process suggests that successful neural ageing is possible for most people, but also cautions that cures for neurodegenerative disorders are unlikely in the near future.
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Selective neuronal vulnerability to oxidative stress in the brain.
Xinkun Wang,Elias K. Michaelis +1 more
TL;DR: In this review, the currently known molecular and cellular factors that contribute to SNV to OS are summarized and include high intrinsic OS, high demand for ROS/RNS-based signaling, low ATP production, mitochondrial dysfunction, and high inflammatory response in vulnerable neurons.
References
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Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.
TL;DR: This review provides a comprehensive summary on the chemical properties of 4-hydroxyalkenals and malonaldehyde, the mechanisms of their formation and their occurrence in biological systems and methods for their determination, as well as the many types of biological activities described so far.
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Mitochondrial control of cell death
Guido Kroemer,John C. Reed +1 more
TL;DR: In many instances, permeabilization of mitochondrial membranes is a rate-limiting step of apoptotic or necrotic cell demise, which has important consequences for the pathophysiology of cell death, as well as for its pharmacological control.
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Protein oxidation and aging
TL;DR: The importance of protein oxidation in aging is supported by the observation that levels of oxidized proteins increase with animal age and may reflect age-related increases in rates of ROS generation, decreases in antioxidant activities, or losses in the capacity to degrade oxidized protein.
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A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study
Mary Sano,Christopher Ernesto,Ronald G. Thomas,Melville R. Klauber,Kimberly Schafer,Michael Grundman,Peter B. Woodbury,John H. Growdon,Carl W. Cotman,Eric Pfeiffer,Lon S. Schneider,Leon J. Thal +11 more
TL;DR: In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease.
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Oxidative stress hypothesis in alzheimer's disease
TL;DR: Supporting indirect evidence comes from a variety of in vitro studies showing that free radicals are capable of mediating neuron degeneration and death, suggesting that therapeutic efforts aimed at removal of ROS or prevention of their formation may be beneficial in AD.