γ‐Glutamylglutamine and Taurine Concentrations Are Decreased in the Cerebrospinal Fluid of Drug‐Naive Patients with Schizophrenic Disorders

Q., K.; Lauer, Christoph; Schreiber, Wolfgang; Zollinger, Markus; Gutteck-Amsler, Ursula; Cuénod, Michel; Holsboer, Florian

doi:10.1046/j.1471-4159.1995.65062652.x

Cited by 73 publications

(34 citation statements)

References 31 publications

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“…Whether the difference in plasma taurine levels in females depends on the menstrual cycle or on the illness cannot be elucidated from our data. In contrast to Do et al (1995), who found lower taurine levels in the CSF in unmedicated patients with schizophrenia compared with controls, we found no statistically significant differences. Because the patients in our study were medicated and well-controlled outpatients, the mild degree of the disorder found might have an impact on the taurine levels in the CSF.…”

Section: Discussioncontrasting

confidence: 99%

“…Studies, in both blood and CSF, indicate that taurine and GSH levels are altered in patients with schizophrenia compared to healthy individuals (Bjerkenstedt et al, 1985;Rao et al, 1990;Do et al, 1995Do et al, , 2000Raffa et al, 2009). In previous studies, we found complex associations between the taurine (Samuelsson et al, 2009) andGSH (Samuelsson et al 2011) levels in plasma and CSF in healthy men.…”

Section: Introductionmentioning

confidence: 55%

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Taurine and glutathione in plasma and cerebrospinal fluid in olanzapine treated patients with schizophrenia

Samuelsson

Skogh

Lundberg

et al. 2013

Psychiatry Research

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 55%

Taurine and glutathione in plasma and cerebrospinal fluid in olanzapine treated patients with schizophrenia

Samuelsson

Skogh

Lundberg

et al. 2013

Psychiatry Research

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“…Further supportive evidence is provided by a study reporting a 27 % reduction in the CSF glutathione level in neuroleptic-naive patients with schizophrenia compared with controls, which coexisted with a 52 % glutathione reduction in the medial prefrontal cortex, as measured by magnetic resonance spectroscopy (Do et al, 2000). The low CSF glutathione appears to be consistent with previous findings of decreased levels of its metabolite, c-glutamylglutamine, in the CSF of schizophrenia patients (Do et al, 1995).…”

Section: Assays Of Oxidants and Antioxidantssupporting

confidence: 77%

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

865

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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“…Taurine deficiency in development leads to abnormal cerebellar organization and function. Reduced levels of CSF taurine lave been demonstrated in drug-free schizophrenic patients (Do et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Maternal infection leads to abnormal gene regulation and brain atrophy in mouse offspring: Implications for genesis of neurodevelopmental disorders

Fatemi

Reutiman

Folsom

et al. 2008

Schizophrenia Research

241

223

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Prenatal viral infection has been associated with development of schizophrenia and autism. Our laboratory has previously shown that viral infection causes deleterious effects on brain structure and Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public AccessAuthor Manuscript Schizophr Res. Author manuscript; available in PMC 2009 February 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript function in mouse offspring following late first trimester (E9) administration of influenza virus. We hypothesized that late second trimester infection (E18) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring. C57BL6J mice were infected on E18 with a sublethal dose of human influenza virus or sham-infected using vehicle solution. Male offsping of the infected mice were collected at P0, P14, P35 and P56, their brains removed and prefrontal cortex, hippocampus and cerebellum dissected and flash frozen. Microarray, qRT-PCR, DTI and MRI scanning, western blotting and neurochemical analysis were performed to detect differences in gene expression and brain atrophy. Expression of several genes associated with schizophrenia or autism including Sema3a, Trfr2 and Vldlr were found to be altered as were protein levels of Foxp2. E18 infection of C57BL6J mice with a sublethal dose of human influenza virus led to significant gene alterations in frontal, hippocampal and cerebellar cortices of developing mouse progeny. Brain imaging revealed significant atrophy in several brain areas and white matter thinning in corpus callosum. Finally, neurochemical analysis revealed significantly altered levels of serotonin (P14, P35), 5-Hydroxyindoleacetic acid (P14) and taurine (P35). We propose that maternal infection in mouse provides an heuristic animal model for studying the environmental contributions to genesis of schizophrenia and autism, two important examples of neurodevelopmental disorders.

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γ‐Glutamylglutamine and Taurine Concentrations Are Decreased in the Cerebrospinal Fluid of Drug‐Naive Patients with Schizophrenic Disorders

Abstract: HPLC and gas chromatography-mass spec-

Cited by 73 publications

References 31 publications

Taurine and glutathione in plasma and cerebrospinal fluid in olanzapine treated patients with schizophrenia

Taurine and glutathione in plasma and cerebrospinal fluid in olanzapine treated patients with schizophrenia

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Maternal infection leads to abnormal gene regulation and brain atrophy in mouse offspring: Implications for genesis of neurodevelopmental disorders

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