Chapter 11 - Pathophysiology and clinical implementation of traumatic brain injury biomarkers: neuron-specific enolase

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Abstract

Neuron-specific enolase (NSE) is an essential protein most recognized for its enzymatic properties during the late stages of glycolysis. NSE has a myriad of other cellular functions and acts primarily on neuronal and neuroendocrine tissues. Under normal physiological conditions, NSE is not secreted into extracellular space, however, during cellular injury or death, NSE can be both leaked into the extracellular space and upregulated in response to the damaged neuronal tissue. NSE has been used as a biomarker in numerous pathological conditions in humans. For decades, NSE assessment has been notable for its usefulness in patients who have certain neuroendocrine malignancies or those who suffer from hypoxic brain damage due to cardiac arrest or ischemic stroke. Additionally, as scientists and clinicians work to risk stratify and guide prognosis in traumatic brain and spinal cord injuries, NSE assessment has shown promise as a biomarker. Though elevated serum levels of NSE in patients after mild traumatic brain injury (TBI) have been reported in multiple studies, the single use of NSE for risk stratification or outcome prognosis in mild TBI appears to have limitations. In severe TBI, higher NSE concentrations are associated with elevated intracranial pressure, severity of traumatic brain damage, adverse outcomes, and mortality. Albeit promising, there remains a lack of standardization with regards to timing of the blood sampling, cutoff ranges and assays when utilizing NSE as a biomarker for traumatic brain injury.

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    GFAP is the major intermediate filament protein in astrocytes which plays a critical role in neurotransmitter homeostasis and cytoskeleton formation (Cheng et al., 2019). Enolase 2 (ENO2), a well-established tumour biomarker for brain damage, is responsible for the conversion of 2- phosphoglycerate (2-PGA) to phosphoenolpyruvate (PEP) [4]. In this study, GFAP and ENO2 were significantly upregulated upon DEP exposure (Figs. 12 and 13) [20].

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