Serum S100B Is Related to Illness Duration and Clinical Symptoms in Schizophrenia—A Meta-Regression Analysis

Abstract

S100B has been linked to glial pathology in several psychiatric disorders. Previous studies found higher S100B serum levels in patients with schizophrenia compared to healthy controls, and a number of covariates influencing the size of this effect have been proposed in the literature. Here, we conducted a meta-analysis and meta-regression analysis on alterations of serum S100B in schizophrenia in comparison with healthy control subjects. The meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement to guarantee a high quality and reproducibility. With strict inclusion criteria 19 original studies could be included in the quantitative meta-analysis, comprising a total of 766 patients and 607 healthy control subjects. The meta-analysis confirmed higher values of the glial serum marker S100B in schizophrenia if compared with control subjects. Meta-regression analyses revealed significant effects of illness duration and clinical symptomatology, in particular the total score of the Positive and Negative Syndrome Scale (PANSS), on serum S100B levels in schizophrenia. In sum, results confirm glial pathology in schizophrenia that is modulated by illness duration and related to clinical symptomatology. Further studies are needed to investigate mechanisms and mediating factors related to these findings.

Higher Plasma S100B Concentrations in Schizophrenia Patients and Dependently Associated with Inflammatory Markers

“…The first finding of this study is that schizophrenia patients have high levels of plasma S100B. Our finding is consistent with the results of numerous previous studies, which consistently found increased concentrations of S100B in blood of patients with schizophrenia 4 10 11 35 36 , although some contravariant reports 14 37 . Peripheral levels of S100B were reported consistence to those of cerebrospinal fluid, and represented a useful peripheral biomarker for brain tissue damages or glial dysfunction.…”

Different serum protein factor levels in first‐episode drug‐naive patients with schizophrenia characterized by positive and negative symptoms

“…Compared to the control subjects, the first-episode drug-naive schizophrenia patients characterized by positive symptoms and those characterized by negative symptoms exhibited increased serum levels of IL-6, IL-1β, and S100β, along with decreased serum levels of NGF and NT-3. These findings confirmed those of previous studies [12][13][14]17,18,30 and may indicate that neurotrophasthenia, increased neuroimmune activation, and damage to glial cells are probably involved in the pathology of schizophrenia. [39][40][41] There is currently no definitive standard for the negative and positive symptom domains.…”

“…In recent decades, in addition to the dopamine hypothesis, the pathophysiology of schizophrenia has been demonstrated to involve neurotrophy, neuroimmunology, and neurodegeneration. 10,11 Studies on peripheral blood serum have also reported that some protein factors are associated with the pathophysiology of schizophrenia, as well as with psychotic symptoms, such as central neurotrophic factors (including nerve growth factor [NGF] 12 and neurotrophin-3 [NT-3] 13 ), neural immune-related proteins (including serum interleukin-6 [IL-6] [14][15][16] and interleukin-1 beta [IL-1β] 17 ), and proteins that are related to the damage of glial cells (including the calcium-binding protein, S100β 16,18 ). Levels of NGF have been found to be decreased in the plasma and cerebrospinal fluid of schizophrenia patients.…”

“…S100β can regulate the proliferation and differentiation of neurons and glia. 31 Studies have demonstrated that serum levels of S100β seem to be significantly higher in schizophrenia patients, 18,32 and increased serum levels of S100β are positively correlated with the negative symptoms of schizophrenia. [33][34][35] To date, accumulating studies have indicated that multiple dysfunctions in dopaminergic, glutamatergic, serotonergic, and gammaaminobutyric acid (GABA)-ergic signaling might be involved in the pathophysiology of schizophrenia.…”

Clinical, cognitive and neuroanatomical associations of serum NMDAR autoantibodies in people at clinical high risk for psychosis

“…There is widespread evidence for BBB disruption in psychotic disorders [28], although human studies are limited by the requirement for CSF samples or the use of proxy clinical markers such as a history of brain injury. One such marker is the astrocytic calcium-binding protein S100B, which is elevated in schizophrenia [28][29][30][31], and can be measured in serum samples alongside autoantibodies.…”