Oxidative Stress, Neuroinflammation, and NADPH Oxidase: Implications in the Pathogenesis and Treatment of Alzheimer's Disease.
Upasana GangulyUpinder KaurSankha Shubhra ChakrabartiPriyanka SharmaBimal Kumar AgrawalSarmistha SahaSasanka ChakrabartiPublished in: Oxidative medicine and cellular longevity (2021)
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.
Keyphrases
- reactive oxygen species
- inflammatory response
- lipopolysaccharide induced
- lps induced
- oxidative stress
- dna damage
- toll like receptor
- cell death
- cognitive decline
- neuropathic pain
- cerebral ischemia
- traumatic brain injury
- high resolution
- multiple sclerosis
- subarachnoid hemorrhage
- induced apoptosis
- mild cognitive impairment
- combination therapy
- immune response
- cognitive impairment
- spinal cord injury
- spinal cord
- signaling pathway
- endoplasmic reticulum stress
- smoking cessation