Abstract
The role of nitric oxide in the pathogenesis and progression of neurodegenerative illnesses such as Parkinson’s and Alzheimer’s diseases has become prominent over the years. Increased activity of the enzymes that produce reactive oxygen species, decreased activity of antioxidant enzymes and imbalances in glutathione pools mediate and mark the neurodegenerative process. Much of the oxidative damage of proteins is brought about by the overproduction of nitric oxide by nitric oxide synthases (NOS) and its subsequent reactivity with reactive oxygen species. Proteomic methods have advanced the field tremendously, by facilitating the quantitative assessment of differential expression patterns and oxidative modifications of proteins and alongside, mapping their non-canonical functions. As a signaling molecule involved in multiple biochemical pathways, the level of nitric oxide is subject to tight regulation. All three NOS isoforms display aberrant patterns of expression in Alzheimer’s disease, altering intracellular signaling and routing oxidative stress in directions that are uncompounded. This review discusses the prime factors that control nitric oxide biosynthesis, reactivity footprints and ensuing effects in the development of neurodegenerative diseases.
Keywords: Alzheimer’s disease, interactome, metal homeostasis, neurodegenerative disease, nitric oxide, NOS, oxidative stress, proteomics.
Current Alzheimer Research
Title:Nitric Oxide Homeostasis in Neurodegenerative Diseases
Volume: 13 Issue: 2
Author(s): Luciana Hannibal
Affiliation:
Keywords: Alzheimer’s disease, interactome, metal homeostasis, neurodegenerative disease, nitric oxide, NOS, oxidative stress, proteomics.
Abstract: The role of nitric oxide in the pathogenesis and progression of neurodegenerative illnesses such as Parkinson’s and Alzheimer’s diseases has become prominent over the years. Increased activity of the enzymes that produce reactive oxygen species, decreased activity of antioxidant enzymes and imbalances in glutathione pools mediate and mark the neurodegenerative process. Much of the oxidative damage of proteins is brought about by the overproduction of nitric oxide by nitric oxide synthases (NOS) and its subsequent reactivity with reactive oxygen species. Proteomic methods have advanced the field tremendously, by facilitating the quantitative assessment of differential expression patterns and oxidative modifications of proteins and alongside, mapping their non-canonical functions. As a signaling molecule involved in multiple biochemical pathways, the level of nitric oxide is subject to tight regulation. All three NOS isoforms display aberrant patterns of expression in Alzheimer’s disease, altering intracellular signaling and routing oxidative stress in directions that are uncompounded. This review discusses the prime factors that control nitric oxide biosynthesis, reactivity footprints and ensuing effects in the development of neurodegenerative diseases.
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Cite this article as:
Hannibal Luciana, Nitric Oxide Homeostasis in Neurodegenerative Diseases, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205012666150921101250
DOI https://dx.doi.org/10.2174/1567205012666150921101250 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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