Traumatic brain injury is a leading cause of morbidity and mortality worldwide, with clinical outcomes varying significantly among individuals. Head injuries are classified based on severity and type of brain damage, significantly impacting cognitive and physical functions. Several factors can influence patient outcomes in TBIs, including age, injury severity, mechanism of injury, abnormalities in computed tomography (CT) imaging, conditions of hypoxia and hypotension, pupil reflexes, and laboratory parameters. This study highlights the critical roles of Apolipoprotein E (APOE), Glial Fibrillary Acidic Protein (GFAP), Phosphorylated Neurofilament Heavy Chain (pNFH), and Neuron Specific Enolase (NSE) in the pathogenesis and recovery of TBIs, providing new insights for targeted therapeutic approaches based on individual genetics. This research is a literature analysis of articles obtained from databases such as Google Scholar, Research Gate, PubMed, and Science Direct. The review of several journals indicates that TBIs involve different genetic variations that play roles in cognitive processes, injury mechanisms, neurodegenerative processes, and repair mechanisms. Glial Fibrillary Acidic Protein (GFAP) is a specific marker for glial cell damage. Phosphorylated Neurofilament Heavy Chain (pNFH) is a specific marker for axonal damage, while Neuron Specific Enolase (NSE) is a specific marker for neuronal damage.