Neurobiology of schizophrenia spectrum disorders: the role of oxidative stress.
- Author:
Stephen J WOOD
1
;
Murat YÜCEL
;
Christos PANTELIS
;
Michael BERK
Author Information
1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne & Melbourne Health, Melbourne, Australia. sjwood@unimelb.edu.au
- Publication Type:Journal Article
- MeSH:
Acetylcysteine;
Glutathione;
Humans;
Magnetic Resonance Imaging;
Mitochondrial Diseases;
Nervous System;
physiopathology;
Oxidative Stress;
Schizophrenia;
physiopathology
- From:Annals of the Academy of Medicine, Singapore
2009;38(5):396-396
- CountrySingapore
- Language:English
-
Abstract:
Mitochondrial dysfunction and oxidative stress are increasingly implicated in the pathophysiology of schizophrenia. The brain is the body's highest energy consumer, and the glutathione system is the brain's dominant free radical scavenger. In the current paper, we review the evidence of central and peripheral nervous system anomalies in the oxidative defences of individuals with schizophrenia, principally involving the glutathione system. This is reflected by evidence of the manifold consequences of oxidative stress that include lipid peroxidation, protein carboxylation, DNA damage and apoptosis - all potentially part of the process of neuroprogression in the disorder. Importantly, oxidative stress is amenable to intervention. We consider the clinical potential of some possible interventions that help reduce oxidative stress, via augmentation of the glutathione system, particularly N-acetyl cysteine. We argue that a better understanding of the mechanisms and pathways underlying oxidative stress will assist in developing the therapeutic potential of this area.
