Validating Serum S100B and Neuron-Specific Enolase as Biomarkers for the Human Brain – A Combined Serum, Gene Expression and MRI Study

Streitbürger, Daniel Paolo; Arélin, Katrin; Kratzsch, Jürgen; Thiery, Joachim; Steiner, Johann; Villringer, Arno; Mueller, Karsten; Schroeter, Matthias L.

doi:10.1371/journal.pone.0043284

Cited by 69 publications

(81 citation statements)

References 73 publications

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“…The finding of positive correlation between S100B and white matter hyperintensities in healthy subjects is in agreement with a study by Streitbuerger et al (2012). These authors reported an association between serum S100B and the diffusion tensor imaging parameters fractional anisotropy and radial diffusivity in white matter tracts in healthy females.…”

Section: Discussionsupporting

confidence: 92%

“…The differences between our and the former study might be attributed to the differences in the studied samples with regard to disease severity and age. Further studies are in agreement with our finding for healthy subjects by showing higher S100B in healthy female than male adults (Streitbuerger et al, 2012) and children (Gazzolo et al, 2003). Overall, the literature on effects of gender on S100B did not reach consensus so far.…”

Section: Discussionsupporting

confidence: 88%

“…S100B and NSE were measured with monoclonal 2-site immunoluminometric assays performed on the fully mechanized system LIAISON (Diasorin, Dietzenbach, Germany). The detection limit for the assays was 0.02 µg/l and 0.04 µg/l (described in detail elsewhere (Streitbuerger et al, 2012). BDNF was measured in serum with an ELISA manufactured by R&D systems (Wiesbaden, Germany).…”

Section: Diagnostic Criteria and Laboratory Proceduresmentioning

confidence: 99%

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First Evidence For Glial Pathology In Late Life Minor Depression: s100b Is Increased In Males With Minor Depression

et al. 2016

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Minor depression is diagnosed when a patient suffers from 2 to 4 depressive symptoms for at least 2 weeks. Though minor depression is a widespread phenomenon, its pathophysiology has hardly been studied. To get a first insight into the pathophysiological mechanisms underlying this disorder we assessed serum levels of biomarkers for plasticity, glial and neuronal function: brain-derived neurotrophic factor (BDNF), S100B and neuron specific enolase (NSE). 27 subjects with minor depressive episode and 82 healthy subjects over 60 years of age were selected from the database of the Leipzig population-based study of civilization diseases (LIFE). Serum levels of BDNF, S100B and NSE were compared between groups, and correlated with age, body-mass index (BMI), and degree of white matter hyperintensities (score on Fazekas scale). S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66). NSE correlated with Fazekas score in patients with minor depression (r s = 0.436, p = 0.048) and in the whole sample (r s = 0.252, p = 0.019). S100B correlated with BMI (r s = 0.246, p = 0.031) and with age in healthy subjects (r s = 0.345, p = 0.002). Increased S100B in males with minor depression, without alterations in BDNF and NSE, supports the glial hypothesis of depression. Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Section: Diagnostic Criteria and Laboratory Proceduresmentioning

confidence: 99%

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First Evidence For Glial Pathology In Late Life Minor Depression: s100b Is Increased In Males With Minor Depression

et al. 2016

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“…Emerging studies have demonstrated that necrosis and apoptosis of brain neurons occur while brain damage is taking place. Neuron-specific enolase (NSE) and S100B have been confirmed to be specific markers of brain damage (3). B7 homolog 3 (B7-H3) is a newly identified member of the B7 superfamily, which serves a key function in the regulation of immune responses (4).…”

Section: Introductionmentioning

confidence: 99%

B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

Chen

Wang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Despite the application of antibiotics, Streptococcus pneumoniae (SP)-induced meningitis continues to be a life-threatening disease with a high fatality rate and an elevated risk of serious neurological sequelae, particularly in developing countries. In this study, the contribution of the co-stimulatory molecule B7 homolog 3 (B7-H3) to the pathogenesis of experimental SP-induced meningitis was investigated. Mice were challenged with the intracerebroventricular injection of serotype 3 SP with or without B7-H3. The clinical status of mice with SP-induced meningitis was examined by body weight loss and spontaneous motor activity with neurological scoring. Coronal brain sections were analyzed by counting Nissl-positive neurons and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells. Protein expression of neuron-specific enolase (NSE) and S100B in brain tissues was examined with immunohistochemical staining. All experiments were performed in a randomized and blinded setting. By the intracerebroventricular injection of SP suspension, a murine model of pneumococcal meningitis was successfully established. In this SP-induced meningitis model, B7-H3 deteriorated the clinical status, as manifested by a decreased neurological score and increased body weight loss. Following the B7-H3 challenge, the number of Nissl-positive cells decreased and TUNEL-stained positive cells increased in the brain tissues of mice with SP meningitis, which demonstrates the enhancement of neuronal necrosis and apoptosis, respectively. Protein expression of NSE was decreased, while that of S100B was increased. These in vivo findings indicate that B7-H3 aggravates brain injury during the pathological process of experimental SP-induced meningitis. IntroductionDespite treatment with effective antibiotics, Streptococcus pneumoniae (SP) meningitis remains a serious infectious disease of the central nervous system (CNS) with mortality rates between 16 and 37% (1) and neurological sequelae in up to 30% of survivors (2). Therefore, further study of the pathological mechanisms of SP meningitis and the identification of new means of intervention has a great clinical significance. SP-induced meningitis can cause disruption of the blood-brain barrier (BBB), and most severely it can result in brain damage, which affects the prognosis of patients with SP meningitis. Emerging studies have demonstrated that necrosis and apoptosis of brain neurons occur while brain damage is taking place. Neuron-specific enolase (NSE) and S100B have been confirmed to be specific markers of brain damage (3). B7 homolog 3 (B7-H3) is a newly identified member of the B7 superfamily, which serves a key function in the regulation of immune responses (4). Our previous study (5) found an abnormally high expression level of soluble B7-H3 (sB7H3) protein in children with bacterial meningitis. In a murine model of SP-induced meningitis, we also demonstrated that B7-H3 further augmented the inflammatory response, exacerbated BBB disruption, a...

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“…Most of it is distributed in the CNS and makes up 1.5 % of soluble protein in the brain [3]. NSE concentrates exclusively in the cytoplasm of neurons and may serve as a marker of neuronal damage [4].…”

mentioning

confidence: 99%

Neuron specific enolase as a possible indicator of neuron damage in children with acute meningitis

Pypa

Svistilnik

Moskovko

et al. 2018

ZMJ

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Acute meningitis in children is a common cause of complications and leads to developmental disabilities. That is the reason why it is important to look for possible markers that indicate nerve tissue damage for early diagnosis, their prevention and prognosis of CNS complications.Objective. To examine neuron specific enolase (NSE) and its diagnostic significance as an indicator of neuronal damage in children with acute meningitis. Materials and methods.Blood samples of 40 children with acute meningitis and 30 of healthy children between the ages of 1 month to 18 years old were studied. The measurement of NSE was made from a blood serum during the first 24 hours after hospitalization by the enzyme-linked immunosorbent assay test performing. The degree of impaired consciousness was determined by the Glasgow Coma Scale. The results were processed with the Student's t-test, correlation and regression analysis methods with constructing confidence intervals.Results. NSE levels in children with acute meningitis was 7.6 times higher than the results of healthy children, which was 22.56 ± 1.14 and 2.95 ± 0.16 ng/ml, respectively, (P < 0.0001) (95 % CI; 19.19 to 20.03). CNS complications of the disease in patients were detected in 22 (55 %). Patients with complications had significantly higher level of NSE than patients without complications and it was 25.35 ± 1.61 and 18.60 ± 1.49 ng/ml, respectively, (P < 0.01) (95 % CI; 5.74 to 7.75). Impaired consciousness was observed in 21 (52.5 %) patients. The content of NSE in patients with impaired consciousness was within 20.72 ± 7.33 ng/ml and it was higher than NSE content in patients with normal consciousness that was within 16.56 ± 4.69 ng/ml (P < 0.05) (95 % CI; 0.17 to 8.14). Reliable inverse and strong correlation was detected between the NSE level and the level of consciousness by the Glasgow Coma Scale, where the coefficient of determination R 2 = 0.624 and coefficient of correlation r -0.785 (P < 0.001) (95 % CI; -1.08 to -0.48).Conclusions. Thus, the data indicates that acute meningitis occurs with the brain matter damage. The blood NSE content in acute meningitis can be used as a biochemical marker for the neuronal damage severity and as a prognostic marker for the CNS complications development.Нейрон-специфічна енолаза як можливий показник нейронального пошкодження при гострих менінгітах у дітей Л. В. Пипа, Р. В. Свістільнік, Г. С. Московко, Ю. М. Лисиця, М. М. МургінаГострий менінгіт у дітей -часта причина виникнення ускладнень і розвитку інвалідизації. Тому важливим є пошук можливих маркерів пошкодження нервової тканини для ранньої діагностики та прогнозу ускладнень із боку ЦНС і їх запобігання.Мета роботи -вивчити вміст нейрон-специфічної енолази у крові та її діагностичне значення як показника нейронального пошкодження в дітей із гострими менінгітами.Матеріали та методи. Виконали дослідження зразків крові 40 дітей із гострими менінгітами, 30 здорових дітей віком від 1 місяця до 18 років. Нейрон-специфічну енолазу (НСЕ) визначали в сироватці крові в першу добу пі...

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Validating Serum S100B and Neuron-Specific Enolase as Biomarkers for the Human Brain – A Combined Serum, Gene Expression and MRI Study

Cited by 69 publications

References 73 publications

First Evidence For Glial Pathology In Late Life Minor Depression: s100b Is Increased In Males With Minor Depression

First Evidence For Glial Pathology In Late Life Minor Depression: s100b Is Increased In Males With Minor Depression

B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

Neuron specific enolase as a possible indicator of neuron damage in children with acute meningitis

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