A Critical Analysis of the Role of the Neurotrophic Protein S100B in Acute Brain Injury

Department of Neurosurgery, Georg August University, Göttingen, Germany.
Journal of Neurotrauma (Impact Factor: 3.71). 09/2006; 23(8):1185-200. DOI: 10.1089/neu.2006.23.1185
Source: PubMed


We provide a critical analysis of the relevance of S100B in acute brain injury emphazising the beneficial effect of its biological properties. S100B is a calcium-binding protein, primarily produced by glial cells, and exerts auto- and paracrine functions. Numerous reports indicate, that S100B is released after brain insults and serum levels are positively correlated with the degree of injury and negatively correlated with outcome. However, new data suggest that the currently held view, that serum measurement of S100B is a valid "biomarker" of brain damage in traumatic brain injury (TBI), does not acknowlege the multifaceted release pattern and effect of the blood-brain barrier disruption upon S100B levels in serum. In fact, serum and brain S100B levels are poorly correlated, with serum levels dependent primarily on the integrity of the blood-brain barrier, and not the level of S100B in the brain. The time profile of S100B release following experimental TBI, both in vitro and in vivo, suggests a role of S100B in delayed reparative processes. Further, recent findings provide evidence, that S100B may decrease neuronal injury and/or contribute to repair following TBI. Hence, S100B, far from being a negative determinant of outcome, as suggested previously in the human TBI and ischemia literature, is of potential therapeutic value that could improve outcome in patients who sustain various forms of acute brain damage.

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Available from: Andrea Kleindienst, Dec 25, 2013
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    • "Although the cellular production of S100B is primarily involved in the modulation of the intracellular milieu, S100B is also secreted in a regulated manner, and it is possible to detect it both in brain tissue or in bodily fluids [3,4]. Most S100B studies have been performed in bodily fluids of humans in pathological conditions or in animal pathological models since increased levels of S100B have been positively correlated with brain pathological conditions [5]. For example, S100B was examined in the CSF (cerebrospinal fluid) and serum of adult patients with acute cerebral infarction, meningitis, multiple sclerosis, dementia, and others neurological pathologies678910. "

    Full-text · Article · Jan 2015
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    • "The increased level of S100β in the hippocampus of 81 day-old young rats exposed to LTG and TPM in utero (Fig. 3B1 and B2) appearantly results from upregulation of S100β expression in astrocytes [28], which is likely to be due to neurodegeneration induced by TPM and LTG in utero. It has been suggested that increments of S100β may improve neurogenesis, particularly in the hippocampus [29] and also stimulate glial proliferation and neuronal survival and protect neurons against glutamate excitotoxicity [30]. NCAM is capable of incorporating long chains of α 2,8 polysialic acid (PSA) [31]. "
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    ABSTRACT: Antiepileptic drugs (AED) which are used to treat seizures in pregnant women, infants, and young children may cause cognitive impairment or other uncertain injury. However, the precise mechanisms responsible for the negative effects of new AEDs like lamotrigine (LTG) and topiramate (TPM) in the developing brain are still unclear. To investigate the GFAP, NCAM and S100B levels in the whole brain of newborn rats on postnatal 1 day and in the hippocampus of adult rats to find out the effect of TPM and LTG on cognitive impairment and brain maturation. Twenty eight pregnant rats were randomly divided into 7 groups with 4 animals in each group. The first group, receiving no drugs, was assigned as the control group. The study groups received intraperitoneal TPM or LTG injections in each trimester. Western blot analysis of the GFAP, NCAM and S100B was performed in the offspring. Behavioral tests were performed at postnatal day 75. The rats in the TPM-I and TPM-III groups had a significant impairment in escape latency on the 5th day as compared to the control rats in a Morris water maze test. In addition, in the expression of astrocyte derived markers, GFAP was upregulated, whereas S100β and NCAM were downregulated in the whole brain on postnatal day 1, in offspring exposed to LTG and TPM in utero. The detrimental effects of TPM and LTG appear to be confined particularly to the early stages of brain development. And TPM seems to have a partial role in the cognitive impairment.
    Full-text · Article · Sep 2014 · Advances in Clinical and Experimental Medicine
    • "The levels of S100B are furthermore higher several weeks before the onset of clinical symptoms in women developing pre-eclampsia compared to healthy controls. S100B is most abundant in glial cells of the central nervous system, predominately in astrocytes and the protein has both neurotrophic and neuroprotective effects[12]. The source of the increased amount of circulating S100B in women developing pre-eclampsia cannot be concluded from our study but it is known that women with preeclampsia have cerebral hemodynamic changes, even predating the pre-eclamptic syndrome[18,19]. "

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