The Prognostic Value of Serum Neuron-Specific Enolase in Traumatic Brain Injury: Systematic Review and Meta-Analysis

Cheng, Feng; Yuan, Qiang; Yang, Jian; Wang, Wenming; Liu, Hua

doi:10.1371/journal.pone.0106680

Cited by 117 publications

(99 citation statements)

References 36 publications

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“…NSE, a peripheral marker of neuronal damage, might be either of central (Cheng et al, 2014) or peripheral origin (Li et al, 2013). In major depression a central origin is suggested by the correlation with white matter hyperintensities.…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…Cell-surface expression of enolase is often detected on activated monocytes/macrophages, microglia, and astrocytes, which promotes degradation of extracellular matrix (ECM), production of pro-inflammatory cytokines/chemokines, and invasion of inflammatory cells in the sites of injury (2, 9–11). Upon activation, enolase can also act as a heat-shock protein by binding to cytoskeletal and chromatin structures, and may play crucial roles in a variety of injury, and pathophysiological processes (9, 12, 13). While enolase expression is detected throughout the body, distinct isoforms are found to be tissue specific.…”

Section: Introductionmentioning

confidence: 99%

Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats

et al. 2017

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Spinal cord injury (SCI) is a complex debilitating condition leading to permanent life-long neurological deficits. The complexity of SCI suggests that a concerted multi-targeted therapeutic approach is warranted to optimally improve function. Damage to spinal cord is complicated by an increased detrimental response from secondary injury factors mediated by activated glial cells and infiltrating macrophages. While elevation of enolase especially Neuron Specific Enolase (NSE) in glial and neuronal cells is believed to trigger inflammatory cascades in acute SCI, alteration of NSE and its subsequent effects in acute SCI remains unknown. This study measured NSE expression levels and key inflammatory mediators after acute SCI and investigated the role of ENOblock, a novel small molecule inhibitor of enolase, in a male Sprague-Dawley (SD) rat SCI model. Serum NSE levels as well as cytokines/chemokines and metabolic factors were evaluated in injured animals following treatment with vehicle alone or ENOblock using Discovery assay. Spinal cord samples were also analyzed for NSE and MMPs 2 and 9 as well as glial markers by Western blotting. The results indicated a significant decrease in serum inflammatory cytokines/chemokines and NSE, alterations of metabolic factors and expression of MMPs in spinal cord tissues after treatment with ENOblock (100μg/kg, twice). These results support the hypothesis that activation of glial cells and inflammation status can be modulated by regulation of NSE expression and activity. Analysis of SCI tissue samples by immunohistochemistry confirmed that ENOblock decreased gliosis which may have occurred through reduction of elevated NSE in rats. Overall, elevation of NSE is deleterious as it promotes extracellular degradation and production of inflammatory cytokines/chemokines and metabolic factors which activates glia and damages neurons. Thus, reduction of NSE by ENOblock may have potential therapeutic implications in acute SCI.

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“…Unfortunately, hemolyzed samples show false positives [74]. Recent meta-analyses have shown that NSE can be used as an indicator of functional levels and mortality rates after TBI [75].…”

Section: Nsementioning

confidence: 99%

Current State and Prospects of Development of Blood-based Biomarkers for Mild Traumatic Brain Injury

Lee

Seo

et al. 2017

Brain Neurorehabil

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Highlights• There are many unresolved clinical problems about mild traumatic brain injury (mTBI) such as a low sensitivity of standard neuroimaging studies, and absence of reliable predicting models.• It is very difficult to diagnose mTBI in symptomatic patients in the absence of witnesses, clear signs of head trauma, and abnormalities on neuroimaging.• Blood proteins have great potential as diagnostic and prognostic biomarkers of mTBI.• Technological advances in the targeted proteomics are expected to realize the clinical potential of blood-based protein biomarkers. ABSTRACTThe current understanding of the pathophysiology of mild traumatic brain injury (mTBI) is, without doubt, incomplete. Nevertheless, we tried to summarize the state-of-the-art explanation of how the brain is continuously injured even after a single impact. We also reviewed the real struggle of diagnosing mTBI, which culminated in showing the potential of blood-based biomarkers as an alternative or complementary way to overcome this difficulty. Pathophysiology of mTBI is subdivided into primary and secondary injuries. Primary injury is caused by a direct impact on the head and brain. Secondary injury refers to the changes in energy metabolism and protein synthesis/degradation resulting from the biochemical cascades as follows; calcium influx, mitochondrial dysfunction, fractured microtubules, and Wallerian degeneration, neuroinflammation, and toxic proteinopathy. Since the diagnosis of mTBI is made through the initial clinical information, it is difficult and inaccurate to diagnose mTBI without the absence of a witness or sign of head trauma. Blood-based biomarkers are expected to play an important role in diagnosing mTBI and predicting functional outcomes, due to their feasibility and the recent progress of targeted proteomics techniques (i.e., liquid chromatography tandem mass spectrometry [LC-MS/MS]).

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The Prognostic Value of Serum Neuron-Specific Enolase in Traumatic Brain Injury: Systematic Review and Meta-Analysis

Cited by 117 publications

References 36 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

Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats

Current State and Prospects of Development of Blood-based Biomarkers for Mild Traumatic Brain Injury

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