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Very important cell types in the brain, aside from neurons, are the neuroglia. These cell types are broadly recognized as having a supportive role. There are 6 types of neuroglia, each with their own function [[File:Types-of-neuroglia_brain-physiology-cells-QBI.png|thumb|250px|Types of glia. <ref name="Arti16">https://qbi.uq.edu.au/brain-basics/brain/brain-physiology/types-glia</ref>]]. In the central nervous system (CNS), the astrocytes are a main type of glial cells. They contribute to the maintenance of homeostasis in the CNS through reactive astrogliosis.<ref name="Arti14">Sofroniew, M. V., & Vinters, H. V. (2009). Astrocytes: biology and pathology. Acta Neuropathologica, 119(1), 7–35. https://doi.org/10.1007/s00401-009-0619-8 </ref> This process is triggered by all types of brain insults and has features that aid recovery, but simultaneously have a potential to inflict damage on the brain. For example, the astrocytes break down their glycogen to supply adjacent neurons with lactate, which the neurons use as fuel to recover. However, the astrocytes also play a critical role in water movements through the brain and in pathological conditions, this can mediate oedema. In all cases of reactive astrogliosis, GFAP is up-regulated. The degree to which the GFAP expression changes, is only dependent on the severity of the trauma to the CNS and not on the morphological appearance of the reactive astrogliosis. <ref name="Arti15">Verkhratsky, A., & Butt, A. (2013). General Pathophysiology of Neuroglia. In Glial Physiology and Pathophysiology (1st ed.). John Wiley & Sons, Ltd. https://doi.org/10.1002/9781118402061 </ref>
When the cause of the increase in GFAP production is brain injury, one can imagine there are several ways for the molecule to end up in the extracellular space instead of remaining in the intracellular space where it was produced [[File:Expression of GFAP in reactive astrogliosis.png|thumb|250px|Expression of GFAP in reactive astrogliosis.<ref name="Arti18">Verkhratsky, A., & Butt, A. (2013). General Pathophysiology of Neuroglia. In Glial Physiology and Pathophysiology (1st ed.). John Wiley & Sons, Ltd. https://doi.org/10.1002/9781118402061</ref>]]. To give an example, necrosis leads to leakage of cellular molecules.<ref name="Arti19">Messing, A., & Brenner, M. (2020). GFAP at 50. ASN Neuro, 12, 175909142094968. https://doi.org/10.1177/1759091420949680</ref> Due to the greater permeability of the BBB, GFAP concentrations increase in the blood as well. Within the first hour of injury, elevated levels of serum GFAP can be detected. At twenty hours of injury, the serum level of GFAP reaches its peak. During the next 52 hours, the GFAP level will decrease slowly. Moreover, there is no significant increase in serum levels of GFAP in patients without TBI.<ref name="Arti17">Abdelhak, A., Foschi, M., Abu-Rumeileh, S., Yue, J. K., D’Anna, L., Huss, A., Oeckl, P., Ludolph, A. C., Kuhle, J., Petzold, A., Manley, G. T., Green, A. J., Otto, M., & Tumani, H. (2022). Blood GFAP as an emerging biomarker in brain and spinal cord disorders. Nature Reviews Neurology, 18(3), 158–172. https://doi.org/10.1038/s41582-021-00616-3</ref> Therefore, a biosensor that detects the levels of GFAP can be used to determine the presence of traumatic brain injury in patients who have received a significant force to their head.
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