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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. 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 provide hope that this approach could lead to novel therapeutic options for the treatment of AD.

Item Type:	Refereed Article
Keywords:	Alzheimer's disease, oxidative stress,
Research Division:	Medical and Health Sciences
Research Group:	Neurosciences
Research Field:	Cellular Nervous System
Objective Division:	Health
Objective Group:	Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:	Nervous System and Disorders
Author:	Chhetri, J (Ms Jamuna Chhetri)
Author:	King, AE (Associate Professor Anna King)
Author:	Gueven, N (Dr Nuri Guven)
ID Code:	114304
Year Published:	2018
Web of Science® Times Cited:	3
Deposited By:	Wicking Dementia Research and Education Centre
Deposited On:	2017-02-10
Last Modified:	2018-04-17
Downloads:	0