Abstract: Traumatic brain injury (TBI) is a temporary or permanent disruption of brain function caused by external forces. TBI has been recognized as an important risk factor for the development of Alzheimer’s disease  and dementia later in life. However, the mechanisms by which TBI contributes to developing Alzheimer’s disease are largely unknown. In particular, no effective therapies are currently available for the prevention and treatment of TBI-induced neurodegenerative disease. The acute brain damage after TBI results not only from primary injury, which is the result of the external mechanical force but also from secondary injury, which is associated with a complex cascade of molecular, cellular, and immune responses. Neuroinflammation associated with other processes plays a critical role in causing secondary injury following TBI (Simon et al., 2017). The extent of neuroinflammatory responses seems to be closely correlated with the outcome following TBI (Woodcock and Morganti-Kossmann, 2013). This means that while the primary injury immediately following TBI is not preventable, appropriate and timely intervention to resolve neuroinflammation following the primary injury would be the key to preventing further brain damage, neuropathological changes, and synaptic and cognitive impairments (Zhang et al., 2015).