MOLECULAR FACTORS IN THE DEVELOPMENT OF NEUROINFLAMMATION IN TRAUMATIC BRAIN INJURY

Abstract

Traumatic brain injury is one of the main causes of both acute and long-term morbidity in the human population. A large number of preclinical and clinical studies do not provide a full description and understanding of the pathophysiological processes occurring during traumatic brain injury and the neuroinflammation it initiates. The neuroinflammatory reaction is a very complex interaction between cells of the innate and adaptive immune systems. The innate immune system is activated by nonspecific danger signals released from damaged cells and tissues, which in turn leads to neutrophil filtration, activation of microglia and astrocytes, release of complement, as well as histamine release by mast cells. We have presented a review of biomarkers and their role in predicting outcomes in traumatic brain injury. Among the biomarkers considered in this article, the most specific for traumatic brain injury and neuroinflammation are interleukin-6, interleukin-8, interleukin-10, and matrix metalloproteinases. Data on other indicators considered in the article are insufficient to use them as specific biomarkers for traumatic brain injury. For a more objective assessment of the patient's condition, several biomarkers should be determined in combination, as the complex of indicators allows a more complete assessment of the condition of the patient with traumatic brain injury.