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Curr Alzheimer Res. 2016;13(2):135-49.

Nitric Oxide Homeostasis in Neurodegenerative Diseases.

Author information

1
Department of Pathobiology, Lerner Research Institute, Cleveland Clinic. 9500 Euclid Ave., Cleveland 44195, USA; Lehrstuhl für Bioanorganische Chemie, Department Chemie und Pharmazie, Universität Erlangen-Nürnberg. Egerlandstraße 1, D-91058 Erlangen, Germany; Departamento de Bioquímica and Centro de Investigaciones Biomédicas (CEINBIO), Facultad de Medicina, Universidad de la República, Avda. General Flores 2125, 11800 Montevideo, Uruguay. mhanniba@kent.edu.

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.

PMID:
26391043
[Indexed for MEDLINE]

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