<scp>S100B</scp> and schizophrenia

Yelmo-Cruz, S.; Fumero, Armando Morera; Abreu-González, Pedro

doi:10.1111/pcn.12024

Cited by 46 publications

(28 citation statements)

References 76 publications

(238 reference statements)

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“…119, 120 Moreover, one of the triggers of M1 activation, S100B, is present at higher levels in individuals with schizophrenia. 121 A parallel is seen here with childhood trauma in which raised levels of pro-inflammatory IL-6 and TNF-a, 122 and reductions in brain-derived neurotrophic factor expression (a product of the M2 pathway) have been observed. 118, 120 …”

Section: Schizophrenia and Microgliasupporting

confidence: 62%

Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization

2017

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An interaction between external stressors and intrinsic vulnerability is one of the longest standing pathoaetiological explanations for schizophrenia. However, novel lines of evidence from genetics, preclinical studies, epidemiology and imaging have shed new light on the mechanisms that may underlie this, implicating microglia as a key potential mediator. Microglia are the primary immune cells of the central nervous system. They have a central role in the inflammatory response, and are also involved in synaptic pruning and neuronal remodeling. In addition to immune and traumatic stimuli, microglial activation occurs in response to psychosocial stress. Activation of microglia perinatally may make them vulnerable to subsequent overactivation by stressors experienced in later life. Recent advances in genetics have shown that variations in the complement system are associated with schizophrenia, and this system has been shown to regulate microglial synaptic pruning. This suggests a mechanism via which genetic and environmental influences may act synergistically and lead to pathological microglial activation. Microglial overactivation may lead to excessive synaptic pruning and loss of cortical gray matter. Microglial mediated damage to stress-sensitive regions such as the prefrontal cortex and hippocampus may lead directly to cognitive and negative symptoms, and account for a number of the structural brain changes associated with the disorder. Loss of cortical control may also lead to disinhibition of subcortical dopamine—thereby leading to positive psychotic symptoms. We review the preclinical and in vivo evidence for this model and consider the implications this has for treatment, and future directions.

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Section: Schizophrenia and Microgliasupporting

confidence: 62%

Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization

2017

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“…34 For example, astrocyte has a protein called S100B, of which there is a significant amount in schizophrenia patients, 35 which makes astrocyte a promising biomarker to predict first episode schizophrenia in the future. 36 Therefore, glial cells have become a major source to supply pathophysiological significance and possible therapeutic target. To investigate the individual contributions made by glial cells in the mechanism and treatment of schizophrenia, our advanced inertial microchip is a promising candidate for isolating glial cells from primary cell cultures.…”

Section: Discussionmentioning

confidence: 99%

A label-free and high-throughput separation of neuron and glial cells using an inertial microfluidic platform

et al. 2016

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While neurons and glial cells both play significant roles in the development and therapy of schizophrenia, their specific contributions are difficult to differentiate because the methods used to separate neurons and glial cells are ineffective and inefficient. In this study, we reported a high-throughput microfluidic platform based on the inertial microfluidic technique to rapidly and continuously separate neurons and glial cells from dissected brain tissues. The optimal working condition for an inertial biochip was investigated and evaluated by measuring its separation under different flow rates. Purified and enriched neurons in a primary neuron culture were verified by confocal immunofluorescence imaging, and neurons performed neurite growth after separation, indicating the feasibility and biocompatibility of an inertial separation. Phencyclidine disturbed the neuroplasticity and neuron metabolism in the separated and the unseparated neurons, with no significant difference. Apart from isolating the neurons, purified and enriched viable glial cells were collected simultaneously. This work demonstrates that an inertial microchip can provide a label-free, high throughput, and harmless tool to separate neurological primary cells. Published by AIP Publishing. [http://dx

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“…A recent review [44] expressed the opinion that S100B studies have been tainted by bias due to selection of patients with high negative symptom levels. Nevertheless, certain explanations for a true positive association between S100B and negative symptoms could be conceived.…”

Section: Discussionmentioning

confidence: 99%

Replicated Evidence of Absence of Association between Serum S100B and (Risk of) Psychotic Disorder

Leeuw

Peeters

Verbeek³

et al. 2013

PLoS ONE

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BackgroundS100B is a potential marker of neurological and psychiatric illness. In schizophrenia, increased S100B levels, as well as associations with acute positive and persisting negative symptoms, have been reported. It remains unclear whether S100B elevation, which possibly reflects glial dysfunction, is the consequence of disease or compensatory processes, or whether it is an indicator of familial risk.MethodsSerum samples were acquired from two large independent family samples (n = 348 and n = 254) in the Netherlands comprising patients with psychotic disorder (n = 140 and n = 82), non-psychotic siblings of patients with psychotic disorder (n = 125 and n = 94) and controls (n = 83 and n = 78). S100B was analyzed with a Liaison automated chemiluminescence system. Associations between familial risk of psychotic disorder and S100B were examined.ResultsResults showed that S100B levels in patients (P) and siblings (S) were not significantly different from controls (C) (dataset 1: P vs. C: B = 0.004, 95% CI −0.005 to 0.013, p = 0.351; S vs. C: B = 0.000, 95% CI −0.009 to 0.008, p = 0.926; and dataset 2: P vs. C: B = 0.008, 95% CI −0.011 to 0.028, p = 0.410; S vs. C: B = 0.002, 95% CI −0.016 to 0.021, p = 0.797). In patients, negative symptoms were positively associated with S100B (B = 0.001, 95% CI 0.000 to 0.002, p = 0.005) in one of the datasets, however with failure of replication in the other. There was no significant association between S100B and positive symptoms or present use or type of antipsychotic medication.ConclusionsS100B is neither an intermediate phenotype, nor a trait marker for psychotic illness.

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S100B and schizophrenia

Cited by 46 publications

References 76 publications

Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization

Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization

A label-free and high-throughput separation of neuron and glial cells using an inertial microfluidic platform

Replicated Evidence of Absence of Association between Serum S100B and (Risk of) Psychotic Disorder

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