Traumatic brain injuries (TBI) are common following head trauma, often leading to short- and long-term complications, including cognitive impairments and neurodegenerative consequences. This review highlights the role of reactive astrocytes in neuroinflammation and neurodegeneration following TBI. Reactive astrocytes, characterized by markers such as glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3), and S100A10, can lead to white-matter inflammation and hyperintensities on MRI scans. Other white-matter changes include increased cortical thickness. The review discusses the gaps in human post-mortem studies and the potential use of these proteins as markers for future research. Understanding the role of reactive astrocytes in TBI may aid in managing patients with TBI and preventing neurodegenerative diseases.Traumatic brain injuries (TBI) are common following head trauma, often leading to short- and long-term complications, including cognitive impairments and neurodegenerative consequences. This review highlights the role of reactive astrocytes in neuroinflammation and neurodegeneration following TBI. Reactive astrocytes, characterized by markers such as glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3), and S100A10, can lead to white-matter inflammation and hyperintensities on MRI scans. Other white-matter changes include increased cortical thickness. The review discusses the gaps in human post-mortem studies and the potential use of these proteins as markers for future research. Understanding the role of reactive astrocytes in TBI may aid in managing patients with TBI and preventing neurodegenerative diseases.