Despite decades of intense research and development, current treatments for schizophrenia
(SZ) have not only met with limited efficacy but are also often associated with serious
side effects, justifying the heightened interest in the development of alternate therapies
(
1
). With mounting experimental evidence implicating glutathione (GSH) deficiency and
increased oxidative stress in the pathophysiology of most major psychiatric disorders
(
2
), novel neuroprotective strategies that aim to limit oxidative stress-mediated cellular
damage in such disorders, including SZ, are being increasingly scrutinized (
2
,
3
).To read this article in full you will need to make a payment
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References
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- Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo.Eur J Neurosci. 2000; 12: 3721-3728
- N-acetylcysteine normalizes neurochemical changes in the glutathione-deficient schizophrenia mouse model during development.Biol Psychiatry. 2012; 71: 1006-1014
- Regulation of glutathione synthesis.Mol Aspects Med. 2009; 30: 42-59
- Glutathione and Parkinson's disease: is this the elephant in the room?.Biomed Pharmacother. 2008; 62: 236-249
- Beneficial effects of N-acetylcysteine in treatment resistant schizophrenia.World J Biol Psychiatry. 2009; 10: 626-628
- N-acetyl cysteine add-on treatment for bipolar II disorder: a subgroup analysis of a randomized placebo-controlled trial.J Affect Disord. 2011; 129: 317-320
- N-acetyl cysteine restores brain glutathione loss in combined 2-cyclohexene-1-one and D-amphetamine-treated rats: relevance to schizophrenia and bipolar disorder.Neurosci Lett. 2011; 499: 149-153
Article info
Publication history
Accepted:
March 29,
2012
Received:
March 28,
2012
Identification
Copyright
© 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
- N-Acetylcysteine Normalizes Neurochemical Changes in the Glutathione-Deficient Schizophrenia Mouse Model During DevelopmentBiological PsychiatryVol. 71Issue 11
- PreviewGlutathione (GSH) is the major cellular redox-regulator and antioxidant. Redox-imbalance due to genetically impaired GSH synthesis is among the risk factors for schizophrenia. Here we used a mouse model with chronic GSH deficit induced by knockout (KO) of the key GSH-synthesizing enzyme, glutamate-cysteine ligase modulatory subunit (GCLM).
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