Purpose of the Review <p>The main objective of this review is to understand the pathological mechanisms involved in the progression of Traumatic brain injury (TBI) and to determine potential therapies showing neuroprotective effects in TBI.</p> Recent Findings <p>Traumatic Brain Injury, particularly in children and young adults, is a major reason of fatality and disability worldwide. Following TBI, a number of pathogenic processes, including excitotoxicity, mitochondrial dysfunction, neuroinflammation, and oxidative stress begin. Two types of damage are produced after TBI, i.e., primary injury and secondary injury. Primary brain damage is caused by a direct impact on the head, which is irreversible and cannot be treated. The primary injury is then followed by a secondary injury, which may be reversible and possibly treatable. It causes biochemical, cellular, and physiological events like blood-brain barrier rupture, oedema formation, and excessive intracellular influx of calcium, oxidative stress, an increase in intracranial pressure, excess release of excitatory neurotransmitters, lipid degradation, and the initiation of inflammatory responses, mitochondrial dysfunction, necrosis, and apoptosis. We can determine potential therapies by comprehending the subsequent pathways that arise from traumatic brain injury.</p> Summary <p>The molecular and structural changes lead to functional disabilities, i.e., cognitive disability and motor dysfunction due to TBI. By understanding the cascades of secondary brain injury, we can find out about the multiple therapeutic approaches.</p>