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

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.

Most Effective Combination of Nutraceuticals for Improved Memory and Cognitive Performance in the House Cricket, Acheta domesticus

“…The brain is particularly vulnerable to oxidative stress because of its high metabolic demand [ 17 , 18 ]. Because ROS are highly reactive, they frequently damage macromolecules, which can lead to mitochondrial dysfunction and ultimately neurodegeneration [ 19 , 20 ]. However, polyphenols have well-documented antioxidant and anti-inflammatory effects [ 21 , 22 , 23 ].…”

Novel approaches in schizophrenia-from risk factors and hypotheses to novel drug targets

“…One allelic variant of the GCLC gene is linked to the decreased activity of glutamate-cysteine ligase and schizophrenia. NMDA receptors are regulated by the redox state, and glutathione deficiency induces NMDA receptor hypofunction, which leads to cortical oxidative stress and glutathione decrease[ 36 , 37 ].…”

The Role of G Protein-Coupled Receptors (GPCRs) and Calcium Signaling in Schizophrenia. Focus on GPCRs Activated by Neurotransmitters and Chemokines

“…High level of oxidative stress has been reported in peripheral blood cells, neutrophils, platelets, cerebrospinal fluid, and post-mortem brain in patients with schizophrenia [ 27 , 28 ]. Oxidative stress is intimately linked to a variety of pathophysiological processes, such as inflammation, oligodendrocyte abnormalities, and mitochondrial dysfunction [ 29 , 30 , 31 ]. An important component in brain pathophysiology is Ca 2+ /CaM-regulated nitric oxide synthase (NOS), which synthesizes nitric oxide (NO) and promotes further generation of a number of reactive oxygen and nitrogen species [ 32 , 33 , 34 ].…”