Oxidative Stress and Antioxidants in Neurodegenerative Disorders

Neurodegenerative disorders constitute a substantial proportion of neurological diseases with significant public health importance. The pathophysiology of neurodegenerative diseases is characterized by a complex interplay of various general and disease-specific factors that lead to the end point of neuronal degeneration and loss, and the eventual clinical manifestations. Oxidative stress is the result of an imbalance between pro-oxidant species and antioxidant systems, characterized by an elevation in the levels of reactive oxygen and reactive nitrogen species, and a reduction in the levels of endogenous antioxidants. Recent studies have increasingly highlighted oxidative stress and associated mitochondrial dysfunction to be important players in the pathophysiologic processes involved in neurodegenerative conditions. In this article, we review the current knowledge of the general effects of oxidative stress on the central nervous system, the different specific routes by which oxidative stress influences the pathophysiologic processes involved in Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis and Huntington's disease, and how oxidative stress may be therapeutically reversed/mitigated in order to stall the pathological progression of these neurodegenerative disorders to bring about clinical benefits.

Automated summary

Neurodegenerative disorders are a significant aspect in neurological diseases, with a pivotal role in public health. The pathophysiology involves the complex interaction between general and disease-specific factors leading to neuronal degeneration and clinical manifestations. Oxidative stress, characterized by an imbalance between pro-oxidant species and antioxidants, has been identified as a crucial factor in the progression of neurodegenerative conditions. This article reviews the impact of oxidative stress on the central nervous system and its influence on Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis, and Huntington's disease, and discusses potential therapeutic approaches to mitigate oxidative stress and halt disease progression for clinical benefits.