4.7 Review

Oxidative stress in schizophrenia: An integrated approach

Journal

NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
Volume 35, Issue 3, Pages 878-893

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2010.10.008

Keywords

Schizophrenia; Oxidative stress; Antioxidant; Immune response; Parvalbumin; N-Methyl-D-aspartate receptor

Funding

  1. NIH [MH080272, MH076060, MH082235]
  2. NATIONAL INSTITUTE OF MENTAL HEALTH [R21MH082235, R01MH076060, P50MH080272] Funding Source: NIH RePORTER

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Oxidative stress has been suggested to contribute to the pathophysiology of schizophrenia. In particular, oxidative damage to lipids, proteins, and DNA as observed in schizophrenia is known to impair cell viability and function, which may subsequently account for the deteriorating course of the illness. Currently available evidence points towards an alteration in the activities of enzymatic and nonenzymatic antioxidant systems in schizophrenia. In fact, experimental models have demonstrated that oxidative stress induces behavioral and molecular anomalies strikingly similar to those observed in schizophrenia. These findings suggest that oxidative stress is intimately linked to a variety of pathophysiological processes, such as inflammation, oligodendrocyte abnormalities, mitochondrial dysfunction, hypoactive N-methyl-D-aspartate receptors and the impairment of fast-spiking gamma-aminobutyric acid interneurons. Such self-sustaining mechanisms may progressively worsen producing the functional and structural consequences associated with schizophrenia. Recent clinical studies have shown antioxidant treatment to be effective in ameliorating schizophrenic symptoms. Hence, identifying viable therapeutic strategies to tackle oxidative stress and the resulting physiological disturbances provide an exciting opportunity for the treatment and ultimately prevention of schizophrenia. (C) 2010 Elsevier Ltd. All rights reserved.

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