• Juan C Leza, Borja García-Bueno, Miquel Bioque, Celso Arango, Mara Parellada, Kim Do, Patricio O'Donnell, and Miguel Bernardo.
• Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Complutense University, Madrid, Spain; Department of Pharmacology, Faculty of Medicine, Complutense University, Madrid, Spain; Instituto de Investigación Sanitaria (IIS) Hospital 12 de Octubre (i+12), Madrid, Spain. Electronic address: jcleza@med.ucm.es.
• Neurosci Biobehav Rev. 2015 Aug 1; 55: 612-26.

AbstractIn the past decade, there has been renewed interest in immune/inflammatory changes and their associated oxidative/nitrosative consequences as key pathophysiological mechanisms in schizophrenia and related disorders. Both brain cell components (microglia, astrocytes, and neurons) and peripheral immune cells have been implicated in inflammation and the resulting oxidative/nitrosative stress (O&NS) in schizophrenia. Furthermore, down-regulation of endogenous antioxidant and anti-inflammatory mechanisms has been identified in biological samples from patients, although the degree and progression of the inflammatory process and the nature of its self-regulatory mechanisms vary from early onset to full-blown disease. This review focuses on the interactions between inflammation and O&NS, their damaging consequences for brain cells in schizophrenia, the possible origins of inflammation and increased O&NS in the disorder, and current pharmacological strategies to deal with these processes (mainly treatments with anti-inflammatory or antioxidant drugs as add-ons to antipsychotics).Copyright © 2015 Elsevier Ltd. All rights reserved.

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