Oxidative Stress, Neuroinflammation, and NADPH Oxidase: Implications in the Pathogenesis and Treatment of Alzheimer’s Disease

Author:

Ganguly Upasana1ORCID,Kaur Upinder2ORCID,Chakrabarti Sankha Shubhra3ORCID,Sharma Priyanka1ORCID,Agrawal Bimal Kumar4ORCID,Saso Luciano5ORCID,Chakrabarti Sasanka1ORCID

Affiliation:

1. Department of Biochemistry, MM Institute of Medical Sciences & Research, Maharishi Markandeshwar Deemed University, Mullana, Ambala, Haryana, India

2. Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

3. Department of Geriatric Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

4. Department of General Medicine, MM Institute of Medical Sciences & Research, Maharishi Markandeshwar Deemed University, Mullana, Ambala, Haryana, India

5. Department of Physiology and Pharmacology “Vittorio Erspamer”, Sapienza University of Rome, Rome, Italy

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.

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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