Traumatic brain injury (TBI) is a common condition that can lead to short- and long-term complications, including neurodegeneration and cognitive impairment. Reactive astrocytes play a significant role in the neuroinflammatory and degenerative processes following TBI. These astrocytes can be classified into neurotoxic and neuroprotective types, with neurotoxic astrocytes contributing to inflammation and neurodegeneration, while neuroprotective astrocytes help in repair and recovery. Markers such as glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3), and S100A10 are used to identify reactive astrocytes. TBI can lead to white-matter hyperintensities and increased cortical thickness, which are associated with cognitive impairments. Studies have shown that TBI is linked to neurodegenerative diseases such as Alzheimer's disease (AD), with chronic traumatic encephalopathy (CTE) and severe TBI showing strong associations with AD pathology. However, the link between mild TBI and neurodegeneration is still under investigation. Neuroinflammation following TBI activates microglia, oligodendrocytes, and astrocytes, leading to neuroprotective and neuroinflammatory responses. The role of reactive astrocytes in TBI is complex, with different gene expressions contributing to neuroinflammation and neurodegeneration. Research on TBI and neurodegeneration is ongoing, with a focus on understanding the mechanisms of astrocyte activation and their impact on brain health. Future studies may explore the use of astrocyte markers in diagnosing and treating TBI-related neurodegeneration.Traumatic brain injury (TBI) is a common condition that can lead to short- and long-term complications, including neurodegeneration and cognitive impairment. Reactive astrocytes play a significant role in the neuroinflammatory and degenerative processes following TBI. These astrocytes can be classified into neurotoxic and neuroprotective types, with neurotoxic astrocytes contributing to inflammation and neurodegeneration, while neuroprotective astrocytes help in repair and recovery. Markers such as glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3), and S100A10 are used to identify reactive astrocytes. TBI can lead to white-matter hyperintensities and increased cortical thickness, which are associated with cognitive impairments. Studies have shown that TBI is linked to neurodegenerative diseases such as Alzheimer's disease (AD), with chronic traumatic encephalopathy (CTE) and severe TBI showing strong associations with AD pathology. However, the link between mild TBI and neurodegeneration is still under investigation. Neuroinflammation following TBI activates microglia, oligodendrocytes, and astrocytes, leading to neuroprotective and neuroinflammatory responses. The role of reactive astrocytes in TBI is complex, with different gene expressions contributing to neuroinflammation and neurodegeneration. Research on TBI and neurodegeneration is ongoing, with a focus on understanding the mechanisms of astrocyte activation and their impact on brain health. Future studies may explore the use of astrocyte markers in diagnosing and treating TBI-related neurodegeneration.