Glial cell dysfunction in schizophrenia indicated by increased S100B in the CSF

Rothermundt, Matthias; Falkai, Peter; Ponath, Gerald; Abel, Simone; Bürkle, Hartmut; Diedrich, M.; Hetzel, Guenter; Peters, Marvin; Siegmund, Ansgar; Pedersen, Anya; Maier, Wolfgang; Schramm, Johannes; Suslow, Thomas; Ohrmann, Patricia; Arolt, Volker

doi:10.1038/sj.mp.4001548

Cited by 138 publications

(56 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…7 The assumption of such extracerebral origins of altered S100B levels in schizophrenia is challenged by findings of elevated S100B in cerebrospinal fluid and postmortem brain tissue. 8,9 However, glial abnormalities in S100B release may also be caused by disrupted energy supply, as suggested by earlier cell culture studies. 2 Accordingly, impaired insulin signaling has been observed in the dorsolateral prefrontal cortex of schizophrenic patients.…”

mentioning

confidence: 74%

Elevated S100B levels in schizophrenia are associated with insulin resistance

et al. 2009

View full text Add to dashboard Cite

mentioning

confidence: 74%

Elevated S100B levels in schizophrenia are associated with insulin resistance

et al. 2009

View full text Add to dashboard Cite

“…Various reports have revealed that altered density and genes due to expressions of astrocytes are strongly related to schizophrenia. 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.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2016

View full text Add to dashboard Cite

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

show abstract

“…Aufgrund der Typ-1-Typ-2-Polarisierung bei Schizophrenie erwartet man im ZNS eine verstärkte Aktivierung von Astrozyten und eine Hemmung der Mikrogliafunktion. Dies zeigt sich in Form von erhöhten Spiegeln von S100B -ein Marker der Astrozytenaktivierung -im Serum und im Liquor schizophrener Patienten, unabhängig vom Medikationsstatus [63,64]. Eine Mikrogliaaktivierung, die bei weniger als 10% schizophrener Patienten zu finden ist, wird als Medikationseffekt diskutiert [3]; vielmehr scheint eine Mikrogliadegeneration bei Schizophrenie mit der Astrozytenaktivierung zu korrespondieren [83].…”

Section: Antipsychotika Rebalancieren Das Typ-1-/typ-2-ungleichgewichtunclassified

Immunology in schizophrenic disorders

Müller

Schwarz

2007

Nervenarzt

View full text Add to dashboard Cite

This manuscript deals with whether immune-mediated mechanisms of inflammation contribute to the pathogenesis of schizophrenia. A model is presented which integrates psychoneuroimmunologic findings and actual results from pharmacological, neurochemical, and genetic studies in schizophrenia. A pivotal role in the neurobiology of schizophrenia is played by dopaminergic neurotransmission, which is modulated by influences of the glutamatergic system. The decreased function of the glutamate system described in schizophrenia seems primarily mediated by N-methyl-D-aspartate (NMDA) receptor antagonism. Kynurenine acid is the only known endogenous NMDA receptor antagonist. In higher concentrations it blocks the NMDA receptor, but in lower concentrations it blocks the nicotinergic acetylcholin receptor, which has a prominent role in cognitive functions. Therefore, higher levels of kynurenine acid may explain psychotic symptoms and cognitive dysfunction. Several findings point out that prenatal infection, associated with an early sensitisation of the immune system, may result in an imbalance of the immune response (type 1 vs type 2) in schizophrenia. This immune constellation leads to inhibition of the enzyme indoleamin dioxigenase (IDO). It and tryptophane 2,3-dioxygenase (TDO) both catalyse the degradation from tryptophan to kynurenine. Due to the inhibition of IDO, tryptophan is metabolised to kynurenine primarily by TDO. In the CNS, TDO is located only in astrocytes, which are in particular activated in schizophrenia and in which kynurenine acid is the final product and can not be further metabolised. Therefore kynurenine acid accumulates in the CNS of schizophrenics and - due to its NMDA-antagonistic properties - leads to cognitive dysfunction and psychotic symptoms. This model describes the pathway of immune-mediated glutamatergic-dopaminergic dysregulation, which may lead to the clinical symptoms of schizophrenia. Therapeutic consequences (e.g. cyclo-oxygenase-2 inhibitors) are discussed.

show abstract

Glial cell dysfunction in schizophrenia indicated by increased S100B in the CSF

Abstract: assessment. On the other hand, the main weakness is that we assessed the suicidal attempters but not suicide completers.In conclusion, given the relatively small sample size of the suicide attempter group in this study, larger samples are needed in future investigations of the TPH2 gene.

Cited by 138 publications

References 10 publications

Elevated S100B levels in schizophrenia are associated with insulin resistance

Elevated S100B levels in schizophrenia are associated with insulin resistance

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

Immunology in schizophrenic disorders

Contact Info

Product

Resources

About