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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|250px270px|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.
== Medical application and relevance ==
The global incidence of TBI is estimated to be 27 to 69 million a year <ref name="Arti20">Dewan, M. C., Rattani, A., Gupta, S., Baticulon, R. E., Hung, Y. C., Punchak, M., Agrawal, A., Adeleye, A. O., Shrime, M. G., Rubiano, A. M., Rosenfeld, J. V., & Park, K. B. (2019). Estimating the global incidence of traumatic brain injury. Journal of Neurosurgery, 130(4), 1080–1097. https://doi.org/10.3171/2017.10.jns17352</ref> <ref name="Arti21">James, S. L., Theadom, A., Ellenbogen, R. G., Bannick, M. S., Montjoy-Venning, W., Lucchesi, L. R., Abbasi, N., Abdulkader, R., Abraha, H. N., Adsuar, J. C., Afarideh, M., Agrawal, S., Ahmadi, A., Ahmed, M. B., Aichour, A. N., Aichour, I., Aichour, M. T. E., Akinyemi, R. O., Akseer, N., . . . Murray, C. J. L. (2019). Global, regional, and national burden of traumatic brain injury and spinal cord injury, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet Neurology, 18(1), 56–87. https://doi.org/10.1016/s1474-4422(18)30415-0</ref>. Across all severities of TBI, mortality is quite low at 3% <ref name="Arti22">Georges, A., & Das, J. M. (2022). Traumatic Brain Injury [Internet]. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459300/</ref> this was determined in the United States of America, a country where the healthcare system is quite developed. While mortality is low, the long term effects of TBI can be detrimental to a person’s quality of life. Some of the acute symptoms lessen or resolve over time, such as dizziness or nausea. Other consequences do not become apparent until a long period of time has passed, for instance psychiatric conditions.<ref name="Arti23">Seel, R. T., Macciocchi, S., & Kreutzer, J. S. (2010). Clinical Considerations for the Diagnosis of Major Depression After Moderate to Severe TBI. Journal of Head Trauma Rehabilitation, 25(2), 99–112. https://doi.org/10.1097/htr.0b013e3181ce3966</ref>
Currently, the Glasgow coma scale (GCS) is the only standardized way to assess patients with a suspected TBI. The GCS provides a practical method for assessing impairment of conscious level in response to defined stimuli.[[File:The glasgow coma scale.png|thumb|250px290px|The Glasgow coma scale.<ref name="Arti24">https://smhs.gwu.edu/urgentmatters/news/keep-it-simple-acute-gcs-score-binary-decision</ref>]] Depending on the final score, the TBI can be classified as minor, moderate or severe.
== References ==
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