ROS and Redox Mechanism in Neurodegenerative Diseases

The prevalence of neurodegenerative diseases has increased in the population, and the pathogenesis of many of these diseases are complex and have yet to be elucidated. Research on exploring the pathogenesis of neuronal loss has implicated OS as a contender of neurodegenerative disease. While mechanisms are complex on what induces OS on these neurodegenerative diseases, it is a common trend of the role of gene expression in down expressing antioxidant genes, OS causing mitochondrial mutations, electron transport chain deficiencies inducing OS, abnormal protein aggregation inducing abnormal metabolic and element use which exacerbates OS and the sensitivity of neurons to OS, due to the presence of PUFA, and reliance on mitochondria that neurons require. Furthermore, the amounting evidence of ROS as both a causative agent and consequence of numerous neurodegenerative diseases highlights its importance in the pathogenesis of these diseases. Research is ongoing and as we delve deeper into the pathophysiology, ROS activity stays a suspect in nearly all neurodegenerative diseases and could play role as a pharmacological and dietary intervention to attenuate the progression of neurodegenerative disease. This article aims to provide an updated role of OS in the abnormal pathogenesis of several neurodegenerative disease, such as Parkinson׳s disease (PD), Alzheimer׳s disease (AD), Huntington׳s disease (HD), amyotrophic lateral sclerosis (ALS), spinocerebellar ataxia disease (SCA).