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Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Author(s)
Madireddy, Sahithi
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Abstract
The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.
Date issued
2020-10-16
URI
https://hdl.handle.net/1721.1/128267
Department
Massachusetts Institute of Technology. Department of Urban Studies and Planning
Journal
Brain Sciences
Publisher
Multidisciplinary Digital Publishing Institute
Citation
Madireddy, Samskruthi and Sahithi Madireddy. “Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia.” Brain Sciences, 10, 10 (October 2020): 742 © 2020 The Author(s) Brain Sciences 10 (10): 742 (2020)
Version: Final published version
ISSN
2076-3425

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