S100B gene polymorphisms predict prefrontal spatial function in both schizophrenia patients and healthy individuals

Zhai, Jing; Cheng, Lijun; Dong, Jicheng; Shen, Qiuge; Zhang, Qiu-Mei; Chen, Min; Gao, Li; Chen, Xiongying; Wang, Keqin; Deng, Xiaoxiang; Xu, Zongbin; Feng, Jia‐Xun; Liu, Chuanxin; Jun, Li; Dong, Qi; Chen, Chuansheng

doi:10.1016/j.schres.2011.09.029

Cited by 18 publications

(18 citation statements)

References 37 publications

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“…The search elicited 40 papers of which eight were reviews. 2,9,22,32,[34][35][36][37] From the 32 non-review papers, eight were focused on genetic studies, [38][39][40][41][42][43][44][45] one paper was focused on the role of S100B protein as a marker of suicidality, 46 another paper focused on S100B and cerebral palsy, 47 one paper was written in Japanese and was related to the levels of S100B in healthy subjects, 48 and another was on histological distribution on S100B immunopositive glia. 13 The latter 12 studies were excluded from the present review.…”

Section: Methodsmentioning

confidence: 99%

S100B and schizophrenia

Yelmo-Cruz

Fumero

Abreu-González

2013

Psychiatry Clin Neurosci

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The research for peripheral biological markers of schizophrenia, although abundant, has been unfruitful. In the last 2 decades, the S100B protein has made its own room in this area of research. S100B is a calcium-binding protein that has been proposed as a marker of astrocyte activation and brain dysfunction. Research results on S100B concentrations and schizophrenia clinical diagnosis are very consistent; patients with schizophrenia have higher S100B concentrations than healthy controls. The results regarding schizophrenia subtypes and clinical characteristics are not as conclusive. Age of patients, body mass index, illness duration and age at onset have been found to show no correlation, a positive correlation or a negative correlation with S100B levels. With respect to psychopathology, S100B data are inconclusive. Positive, negative and absence of correlation between S100B concentrations and positive and negative psychopathology have been reported. Methodological biases, such as day/night and seasonal variations, the use of anticoagulants to treat biological samples, the type of analytical technique to measure S100B and the different psychopathological scales to measure schizophrenia symptoms, are some of the factors that should be taken into account when researching into this area in order to reduce the variability of the reported results. The clinical implications of S100B changes in schizophrenia remain to be elucidated.

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Section: Methodsmentioning

confidence: 99%

S100B and schizophrenia

Yelmo-Cruz

Fumero

Abreu-González

2013

Psychiatry Clin Neurosci

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“…Elevated S100B levels correlate with paranoid [154] and negativistic psychosis [204], impaired cognition, poor therapeutic response and duration of illness [202]. Genetic polymorphisms in S100B [32] and receptor for advanced glycation end-product genes in schizophrenia cohorts (Table 2) [32,33,205] suggest these abnormalities are likely primary/pathogenic rather than secondary/biomarkers. Indeed, the decrease in serum S100B levels following treatment with antidepressants [201] and antipsychotics [196] suggests some clinical relevance of S100B to the pathophysiology of psychiatric disorders.…”

Section: Reviewmentioning

confidence: 99%

Neuroinflammation and psychiatric illness

Najjar

Pearlman

Alper

et al. 2013

J Neuroinflammation

587

473

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Multiple lines of evidence support the pathogenic role of neuroinflammation in psychiatric illness. While systemic autoimmune diseases are well-documented causes of neuropsychiatric disorders, synaptic autoimmune encephalitides with psychotic symptoms often go under-recognized. Parallel to the link between psychiatric symptoms and autoimmunity in autoimmune diseases, neuroimmunological abnormalities occur in classical psychiatric disorders (for example, major depressive, bipolar, schizophrenia, and obsessive-compulsive disorders). Investigations into the pathophysiology of these conditions traditionally stressed dysregulation of the glutamatergic and monoaminergic systems, but the mechanisms causing these neurotransmitter abnormalities remained elusive. We review the link between autoimmunity and neuropsychiatric disorders, and the human and experimental evidence supporting the pathogenic role of neuroinflammation in selected classical psychiatric disorders. Understanding how psychosocial, genetic, immunological and neurotransmitter systems interact can reveal pathogenic clues and help target new preventive and symptomatic therapies.

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“…Astrocyte dysfunction is thus consistent with the hypothesis of neurotransmitter dysfunction in schizophrenia and may contribute to the pathology of schizophrenia. Here we list genes/molecules that are related to schizophrenia from genetics, gene expression, proteomics, and transgenic animal studies (Table ) …”

Section: Astrocytesmentioning

confidence: 99%

Glia‐related genes and their contribution to schizophrenia

Wang

Aleksić

Ozaki

2015

Psychiatry Clin Neurosci

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Schizophrenia, a debilitating disease with 1% prevalence in the general population, is characterized by major neuropsychiatric symptoms, including delusions, hallucinations, and deficits in emotional and social behavior. Previous studies have directed their investigations on the mechanism of schizophrenia towards neuronal dysfunction and have defined schizophrenia as a ‘neuron‐centric’ disorder. However, along with the development of genetics and systematic biology approaches in recent years, the crucial role of glial cells in the brain has also been shown to contribute to the etiopathology of schizophrenia. Here, we summarize comprehensive data that support the involvement of glial cells (including oligodendrocytes, astrocytes, and microglial cells) in schizophrenia and list several acknowledged glia‐related genes or molecules associated with schizophrenia. Instead of purely an abnormality of neurons in schizophrenia, an additional ‘glial perspective’ provides us a novel and promising insight into the causal mechanisms and treatment for this disease.

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S100B gene polymorphisms predict prefrontal spatial function in both schizophrenia patients and healthy individuals

Cited by 18 publications

References 37 publications

S100B and schizophrenia

S100B and schizophrenia

Neuroinflammation and psychiatric illness

Glia‐related genes and their contribution to schizophrenia

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