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Free radical or oxidative stress may be a fundamental mechanism underlying several human neurologic diseases. Therapy using free radical scavengers (antioxidants) has the potential to prevent, delay, or ameliorate many neurologic disorders. However, the biochemistry of oxidative pathobiology is complex, and optimum antioxidant therapeutic options may vary and need to be tailored to individual diseases. In vitro and animal model studies support the potential beneficial role of various antioxidant compounds in neurological disease. Antioxidants generally play an important role in reducing or preventing the cell damage and other changes which occur in the cells like mitochondrial dysfunction, DNA mutations, and lipid peroxidation in the cell membrane. Based on their mechanism of action, antioxidants can be used to treat various neurological disorders like Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease. Vitamin E has a scavenging action for reactive oxygen species (ROS) and also prevents the lipid peroxidation. Creatine generally reduces the mitochondrial dysfunction in Parkinson’s disease (PD) patients. Various metal chelators are used in PD for the prevention of accumulation of the metals. Superoxidase dismutase (SOD), lipases, and proteases act as repair enzymes in patients with AD. Accordingly, the antioxidant defense system is found to be most useful for treating various neurological disorders.
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