Traumatic brain injury (TBI) has been found as the primary cause of morbidity and disability worldwide, which has posed a significant social and economic burden. The first stage of TBI produces brain edema, axonal damage, and hypoxia, thus having an effect on the blood-brain barrier function, promoting inflammatory responses, and increasing oxidative stress. Patients with TBI are more likely to develop post-traumatic epilepsy, behavioral issues, as well as mental illnesses. The long-term effects arising from TBI have aroused rising attention over the past few years. Microglia in the brain can express the triggering receptor expressed on myeloid cells 2 (TREM2), which is a single transmembrane receptor pertaining to the immunoglobulin superfamily. The receptor has been correlated with a number of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and other relevant diseases. In this review, it is demonstrated that TREM2 is promising to serve as a neuroprotective factor for neurodegenerative disorders following TBI by modulating the function of microglial cells. Accordingly, it has potential avenues for TREM2-related therapies to improve long-term recovery after TBI.
Keywords: Microglia; Neurodegenerative Diseases; TBI; The Triggering Receptor Expressed on Myeloid Cells 2.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.