Abstract
NADPH oxidase as an important source of intracellular reactive oxygen species (ROS) has gained enormous importance over the years, and the detailed structures of all the isoenzymes of the NADPH oxidase family and their regulation have been well explored. The enzyme has been implicated in a variety of diseases including neurodegenerative diseases. The present brief review examines the body of evidence that links NADPH oxidase with the genesis and progression of Alzheimer's disease (AD). In short, evidence suggests that microglial activation and inflammatory response in the AD brain is associated with increased production of ROS by microglial NADPH oxidase. Along with other inflammatory mediators, ROS take part in neuronal degeneration and enhance the microglial activation process. The review also evaluates the current state of NADPH oxidase inhibitors as potential disease-modifying agents for AD.
Highlights
A review on oxidative stress and disease mechanisms and therapeutic use of antioxidants is usually not greeted with much enthusiasm, and reasons are not difficult to surmise
There is a considerable body of experimental evidence that suggests the involvement of reactive oxygen species (ROS) and reactive nitrogen species (RNS), generally free radicals of oxygen and nitrogen, in the pathophysiology of many diseases and aging [4,5,6]
This study further demonstrated that treatment with angiotensin II caused cardiac hypertrophy and myocardial fibrosis along with NOX4 upregulation and ROS production in control mice, and all these changes were much more aggravated in human NOX4 transgenic mice (hNOX4) [33]
Summary
A review on oxidative stress and disease mechanisms and therapeutic use of antioxidants is usually not greeted with much enthusiasm, and reasons are not difficult to surmise. The story of oxidative stress and its involvement in multiple disease mechanisms and aging is quite old, spanning many decades [1]. There is a considerable body of experimental evidence that suggests the involvement of reactive oxygen species (ROS) and reactive nitrogen species (RNS), generally free radicals of oxygen and nitrogen, in the pathophysiology of many diseases and aging [4,5,6]. The free radical biology in health and disease has grown gradually over the years from the identification of various species of ROS and RNS in living systems and the elucidation of the chemistry and kinetics of their interactions to the identification of their toxic effects on different biomolecules and cell organelles [7, 8]. The redox-signalling pathways play important roles in cell growth, differentiation, and death as evidenced from a plethora of experimental studies [10,11,12]
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