Abstract
Background: Alzheimer's disease (AD) is a neurodegenerative disease characterised by a progressive decline in cognitive function and represents a major healthcare challenge worldwide. Increasing evidence indicates that mitochondrial dysfunction mediated oxidative stress plays a significant role in the pathophysiological process of AD. Therefore, the physiological activation of antioxidant enzymes that respond to increased oxidative stress is thought to prevent neuropathology. One of those endogenous defences is NADPH quinone oxidoreductase 1 (NQO1). NQO1 is a cytosolic homodimeric flavoprotein that catalyses the two-electron reduction of quinones and related molecules aimed at increasing their solubility and excretion. In line with its role as a phase II stress response protein, altered NQO1 expression is associated with several pathological conditions and disorders including AD.
Conclusion: This review summarizes the association between NQO1 and AD pathology. Understanding this association will provide further insight into the pathogenesis of the disease. More importantly, recent interest in drugs that affect NQO1 expression or its activity provides hope that this approach could lead to novel therapeutic options for the treatment of AD.
Keywords: Alzheimer's disease (AD), NADPH Quinone Oxidoreductase 1 (NQO1), neurofibrillary tangles (NFT), amyloid-β, mitochondrial dysfunction, neurodegenerative disease.
Current Alzheimer Research
Title:Alzheimer's Disease and NQO1: Is there a Link?
Volume: 15 Issue: 1
Author(s): Jamuna Chhetri*, Anna E. King and Nuri Gueven
Affiliation:
- Division of Pharmacy, School of Medicine, Faculty of Health, University of Tasmania, Hobart, TAS 7001,Australia
Keywords: Alzheimer's disease (AD), NADPH Quinone Oxidoreductase 1 (NQO1), neurofibrillary tangles (NFT), amyloid-β, mitochondrial dysfunction, neurodegenerative disease.
Abstract: Background: Alzheimer's disease (AD) is a neurodegenerative disease characterised by a progressive decline in cognitive function and represents a major healthcare challenge worldwide. Increasing evidence indicates that mitochondrial dysfunction mediated oxidative stress plays a significant role in the pathophysiological process of AD. Therefore, the physiological activation of antioxidant enzymes that respond to increased oxidative stress is thought to prevent neuropathology. One of those endogenous defences is NADPH quinone oxidoreductase 1 (NQO1). NQO1 is a cytosolic homodimeric flavoprotein that catalyses the two-electron reduction of quinones and related molecules aimed at increasing their solubility and excretion. In line with its role as a phase II stress response protein, altered NQO1 expression is associated with several pathological conditions and disorders including AD.
Conclusion: This review summarizes the association between NQO1 and AD pathology. Understanding this association will provide further insight into the pathogenesis of the disease. More importantly, recent interest in drugs that affect NQO1 expression or its activity provides hope that this approach could lead to novel therapeutic options for the treatment of AD.
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Cite this article as:
Chhetri Jamuna*, King E. Anna and Gueven Nuri, Alzheimer's Disease and NQO1: Is there a Link?, Current Alzheimer Research 2018; 15 (1) . https://dx.doi.org/10.2174/1567205014666170203095802
DOI https://dx.doi.org/10.2174/1567205014666170203095802 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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