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Oxidative stress in neurology and in neurodegenerative processes

Authors :
Gupta, G
Pathak, S
Rawat, S
Mishra, A
Singh, Y
Mehta, M
Satija, S
Khurana, N
De Jesus Andreoli Pinto, T
Shukla, S
Pabreja, K
Chellappan, DK
Gupta, G
Pathak, S
Rawat, S
Mishra, A
Singh, Y
Mehta, M
Satija, S
Khurana, N
De Jesus Andreoli Pinto, T
Shukla, S
Pabreja, K
Chellappan, DK
Publication Year :
2020

Abstract

Aging is one of the principal risk factors that play an important role in several human conditions and pathogenesis, primarily neurodegenerative disorders, such as amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), and Alzheimer’s disease (AD). A progressive loss of neurons, reduced motor or behavioral functions, and abnormally aggregated proteins define these conditions. An unbalanced redox environment, including the generation of excessive reactive oxygen species (ROS) or system deficiency, causes oxidative stress (OS). The brain is one of the principal organs that are particularly susceptible to ROS because of its elevated oxygen demand and the presence of abundant peroxidation-sensitivelipid cells. Previous studies have reported that widespread neurodegenerative disease pathophysiology involves OS. Cellular antioxidants are known to alter such redox status, target destruction, and regulate oxidative mechanisms engaged in cell proliferation, gene expression, signal transduction, and cell death pathway. Oxidants and antioxidants are important in maintaining free balance, metabolized, environmental-related radicals and the body’s antioxidant mechanisms. In biological systems, several complex natural antioxidant mechanisms occur that work together to prevent prooxidant damage. The objective of this chapter is to demonstrate that free radicals are engaged in neurodegenerative disease pathophysiology and that antioxidants and scavenging products help in the prevention and cure of such disease conditions. This chapter also examines the role of antioxidants in neurodegenerative illnesses, in their chemoprevention and therapy.

Details

Database :
OAIster
Publication Type :
Electronic Resource
Accession number :
edsoai.on1345551129
Document Type :
Electronic Resource