Increased serum S100B in never-medicated and medicated schizophrenic patients

Zhang, Xiang Yang; Xiu, Mei Hong; Song, Cai; Chen, Da Chun; Wu, Gui Ying; Haile, Colin N.; Kosten, Therese A.

doi:10.1016/j.jpsychires.2010.04.023

Cited by 44 publications

(51 citation statements)

References 41 publications

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“…Numerous studies have found evidence for increased levels of pro-inflammatory cytokines and increased microglial activation in patients with schizophrenia, as well as Type 1 T helper (Th1)/Type 2 T helper (Th2) cytokine imbalances involved with immune response (Na et al, 2014). Elevated serum levels of C-reactive protein, a marker of inflammation, have been found in schizophrenia patients with more severe levels of psychopathology (Fan et al, 2007), and elevated serum S100B levels -considered to be the analog of C-reactive protein in the brain -have been found in schizophrenia patients, as well (Sen and Belli, 2007;Zhang et al, 2010).…”

Section: 9mentioning

confidence: 99%

Abnormal immune system development and function in schizophrenia helps reconcile diverse findings and suggests new treatment and prevention strategies

Anders¹,

Kinney

2015

Brain Research

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Section: 9mentioning

confidence: 99%

Abnormal immune system development and function in schizophrenia helps reconcile diverse findings and suggests new treatment and prevention strategies

Anders¹,

Kinney

2015

Brain Research

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“…Another study showed elevated S100B serum levels in both drug-naïve early stage patients and medicated chronic SCZ patients [111], supporting the activation or damage of glial cells in SCZ. Moreover, lower levels of S100B were detected in medicated chronic SCZ patients compared to drug-naïve early stage patients, possibly suggesting that antipsychotic treatment may reduce neurodegeneration or at least the ongoing neuroinflammatory process [111].…”

Section: Cns Biomarkers Candidates In Sczmentioning

confidence: 91%

Biomarkers and schizophrenia: a qualitative review

Silva¹,

Pinto²

2017

IJCNMH

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Schizophrenia (SCZ) is a psychiatric disorder with a broad spectrum of biological and clinical manifestations of yet not completely clear pathophysiological mechanisms. Several lines of evidence have been supporting the idea that immunoinflammatory, oxidative, hormonal and cellular dysfunctions are implicated on the biomolecular basis of SCZ. However, accurate diagnosis and selection of appropriate treatments remains challenging as a result of the scarcity of objective tests. Furthermore, there is a compelling need to find biomarkers that could predict drug response and tailor pharmacological treatment, particularly in drug-naïve first episode psychosis (FEP). Hence, numerous technologies have been employed in order to search for SCZ biological markers, but evidence relating them to treatment efficacy is lacking. In this regard, some preliminary data suggest promising results. The current review provides information on: (1) potential biomarkers associated with biological disturbances and (2) biological markers associated with treatment response.

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“…43,44 Moreover, the S100B protein can be found in glial cells, especially astrocytes, and has been considered as a marker of astrocyte integrity. Increased levels of this protein were found in schizophrenia, particularly in unmedicated patients, 45,46 and also in BD patients, mainly during manic or depressive episodes. 45,47 Because brain tissues use glucose metabolism as their energetic substrate, they are highly dependent on mitochondrial function.…”

Section: Metabolic Systems Involved In the Pathophysiology Of Psychiamentioning

confidence: 95%

The "selfish brain" hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia

Mansur

Brietzke

2012

Trends Psychiatry Psychother.

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A hipótese do "cérebro egoísta" para alterações metabólicas no transtorno bipolar e na esquizofreniaThe "selfish brain" hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia AbstractMetabolic abnormalities are frequent in patients with schizophrenia and bipolar disorder (BD), leading to a high prevalence of diabetes and metabolic syndrome in this population. Moreover, mortality rates among patients are higher than in the general population, especially due to cardiovascular diseases. Several neurobiological systems involved in energy metabolism have been shown to be altered in both illnesses; however, the cause of metabolic abnormalities and how they relate to schizophrenia and BD pathophysiology are still largely unknown. The "selfish brain" theory is a recent paradigm postulating that, in order to maintain its own energy supply stable, the brain modulates energy metabolism in the periphery by regulation of both allocation and intake of nutrients. We hypothesize that the metabolic alterations observed in these disorders are a result of an inefficient regulation of the brain energy supply and its compensatory mechanisms. The selfish brain theory can also expand our understanding of stress adaptation and neuroprogression in schizophrenia and BD, and, overall, can have important clinical implications for both illnesses. Keywords: Schizophrenia, bipolar disorder, metabolism, brain metabolism, stress, allostasis. ResumoAlterações metabólicas são frequentes em pacientes com esquizofrenia e transtorno bipolar (TB), levando a uma alta prevalên-cia de diabetes e síndrome metabólica nessa população. Além disso, as taxas de mortalidade entre pacientes são mais altas do que na população geral, especialmente em decorrência de doenças cardiovasculares. Vários sistemas neurobiológicos envolvidos no metabolismo energético têm demonstrado alterações nas duas doenças; no entanto, a causa das alterações metabó-licas e a forma como elas se relacionam com a fisiopatologia da esquizofrenia e do TB ainda são arenas em grande parte desconhecidas. A teoria do "cérebro egoísta" é um paradigma recente que postula que, para manter estável seu próprio fornecimento de energia, o cérebro modula o metabolismo da energia na periferia regulando tanto a alocação quanto a ingestão de nutrientes. Apresentamos neste artigo a hipótese de que as alterações metabólicas observadas nesses transtornos são resultado de uma regulação ineficiente do fornecimento de energia do cérebro e seus mecanismos compensatórios. A teoria do cérebro egoísta também pode expandir nosso entendimento sobre a adaptação ao estresse e a neuroprogressão na esquizofrenia e no TB, e, acima de tudo, pode ter implicações clínicas importantes para as duas doenças. Descritores: Esquizofrenia, transtorno bipolar, metabolismo, metabolismo cerebral, estresse, alostase.

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Increased serum S100B in never-medicated and medicated schizophrenic patients

Cited by 44 publications

References 41 publications

Abnormal immune system development and function in schizophrenia helps reconcile diverse findings and suggests new treatment and prevention strategies

Abnormal immune system development and function in schizophrenia helps reconcile diverse findings and suggests new treatment and prevention strategies

Biomarkers and schizophrenia: a qualitative review

The "selfish brain" hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia

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