Glial cell activation in a subgroup of patients with schizophrenia indicated by increased S100B serum concentrations and elevated myo-inositol

Rothermundt, Matthias; Ohrmann, Patricia; Abel, Simone; Siegmund, Ansgar; Pedersen, Anya; Ponath, Gerald; Suslow, Thomas; Peters, Marvin; Kaestner, Florian; Heindel, Walter; Arolt, Volker; Pfleiderer, Bettina

doi:10.1016/j.pnpbp.2006.09.013

Cited by 81 publications

(56 citation statements)

References 17 publications

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“…Cerebrospinal fluid and/or plasma S100B is elevated in a number of neurodegenerative diseases including stroke and schizophrenia [28,29,30]. Therefore, the plasma concentration of S100B is often used as a marker of BBB integrity and cerebrovascular inflammation [27,31,32].…”

Section: Methodsmentioning

confidence: 99%

Aging-Related Changes in Blood-Brain Barrier Integrity and the Effect of Dietary Fat

Takechi

Pallebage-Gamarallage

Lam

et al. 2012

Neurodegener Dis

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Background: Disturbances in blood-brain barrier (BBB) integrity contribute to the onset and progression of neurodegenerative diseases including Alzheimer's disease (AD) and vascular dementia (VaD). Aging is positively associated with AD and VaD risk, but this may reflect comorbidities or the effects of other chronic modulators of vascular function such as diet. Objective: To explore putative synergistic effects of aging with diet, in this study genetically unmanipulated mice were maintained on diets enriched in saturated fatty acids (SFA) or cholesterol and compared to mice provided with low-fat (LF) feed formula. Methods: The functional integrity of the BBB was assessed following 3, 6 and 12 months of dietary intervention commenced at 6 weeks of age, by determining the brain parenchymal extravasation of immunoglobulin G (IgG). Results: Mice maintained on the SFA- or cholesterol-enriched diet showed significant parenchymal IgG abundance following 3 months of feeding, concomitant with diminished expression of the tight junction protein occludin. LF control mice had essentially no evidence of BBB disturbances. Six months of SFA feeding exacerbated the difference in IgG abundance compared to the LF mice. At 12 months of feeding, the control LF mice also had significant parenchymal IgG that was comparable to mice fed the SFA- or cholesterol-enriched diet for 3 months. However, there may have been an adaptation to the fat-enriched diets because SFA and cholesterol did not exacerbate IgG parenchymal accumulation beyond 6 months of feeding. Conclusion: Collectively, the study suggests that diets enriched in SFA or cholesterol accelerate the onset of BBB dysfunction that otherwise occurs with aging.

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Section: Methodsmentioning

confidence: 99%

Aging-Related Changes in Blood-Brain Barrier Integrity and the Effect of Dietary Fat

Takechi

Pallebage-Gamarallage

Lam

et al. 2012

Neurodegener Dis

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“…Apart from increased S100B serum levels due to glial cell destruction after brain damage or major inflammation [Lins et al, 2005;Schenatto et al, 2006;Nyl en et al, 2008], S100B cerebrospinal fluid and peripheral blood concentrations were shown to be increased in patients suffering from, for example, Alzheimer's disease, mood disorders and schizophrenia [Peskind et al, 2001;Schroeter et al, 2002Schroeter et al, , 2008Steiner et al, 2006;Rothermundt et al, 2004aRothermundt et al, , 2007. In schizophrenia, elevated S100B levels are associated with negative symptomatology and slower remission upon treatment [Rothermundt et al, 2001[Rothermundt et al, , 2004bSchroeter et al, 2003;Ling et al, 2007].…”

Section: Neuropsychiatric Geneticsmentioning

confidence: 99%

Risk variants in the S100B gene predict elevated S100B serum concentrations in healthy individuals

Hohoff

Ponath

Freitag

et al. 2009

American J of Med Genetics Pt B

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Several lines of evidence suggest an important role of the S100B protein and its coding gene in different neuropathological and psychiatric disorders like dementia, bipolar affective disorders and schizophrenia. To clarify whether a direct link exists between gene and gene product, that is, whether S100B variants directly modulate S100B serum concentration, 196 healthy individuals were assessed for S100B serum concentrations and genotyped for five potentially functional S100B SNPs. Functional variants of the serotonergic genes 5-HT1A and 5-HTT possibly modulating S100B serum levels were also studied. Further, publicly available human postmortem gene expression data were re-analyzed to elucidate the impact of S100B, 5-HT1A and 5-HTT SNPs on frontal cortex S100B mRNA expression. Several S100B SNPs, particularly rs9722, and the S100B haplotype T-G-G-A (including rs2186358-rs11542311-rs2300403-rs9722) were associated with elevated S100B serum concentrations (Bonferroni corrected P < 0.05). Of these, rs11542311 was also associated with S100B mRNA expression directly (Bonferroni corrected P = 0.05) and within haplotype G-A-T-C (rs11542311-rs2839356-rs9984765-rs881827; P = 0.004), again with the G-allele increasing S100B expression. Our results suggest an important role of S100B SNPs on S100B serum concentrations and S100B mRNA expression. It hereby links recent evidence for both, the impact of S100B gene variation on various neurological or psychiatric disorders like dementia, bipolar affective disorders and schizophrenia and the strong relation between S100B serum levels and these disorders.

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“…In in vitro experiments, S100B exerts both detrimental and neurotrophic effects, depending on its concentration in brain tissues [3][4][5] . The plasma levels of S100B were recently found to be slightly increased [3] in psychiatric disorders such as schizophrenia [6][7][8][9][10][11] , major depression [12][13][14] , mania [15] and Alzheimer's disease [3] . A recent meta-analysis by Schroeter et al [14] revealed that S100B serum levels were consistently increased in acute major depressive or manic episodes and decreased during antidepressive treatment if clinical improvement was sufficient.…”

Section: Introductionmentioning

confidence: 99%

S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

Zhang

Rothermundt²,

Peters³

et al. 2009

Neuropsychobiology

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Objective: Memory processes, as reflected by ‘old/new’ effects of event-related potentials (ERPs), have been shown to be impaired in depressed patients. This variability might be partly explained by biological factors. S100B is a glial calcium-binding protein with neuroplastic properties; S100B serum levels have been shown to be increased in depressive patients. The pathophysiologic role of S100B in depression, however, is not yet sufficiently understood. Methods: In the present study, ERPs recorded in a visual continuous word recognition paradigm were therefore investigated in patients with remitted major depression in relation to S100B serum levels. Results: Patients with moderately increased S100B serum levels (n = 6) showed a normal old/new effect in contrast to a reduced old/new effect in patients with normal S100B levels (n = 6) compared to aged-matched controls. Conclusions: These findings provide evidence of an association between S100B levels and memory processes in patients with recurrent depression and further suggest a neuroprotective role of moderately increased S100B serum levels in the course of affective disorders.

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Glial cell activation in a subgroup of patients with schizophrenia indicated by increased S100B serum concentrations and elevated myo-inositol

Cited by 81 publications

References 17 publications

Aging-Related Changes in Blood-Brain Barrier Integrity and the Effect of Dietary Fat

Aging-Related Changes in Blood-Brain Barrier Integrity and the Effect of Dietary Fat

Risk variants in the S100B gene predict elevated S100B serum concentrations in healthy individuals

S100B Serum Levels and Word Memory Processing in Remitted Major Depression as Reflected by Brain Potentials

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