Neuroinflammation and neurodegeneration following traumatic brain injuries.

Abstract

Traumatic brain injuries (TBI) commonly occur following head trauma. TBI may result in short- and long-term complications which may lead to neurodegenerative consequences, including cognitive impairment post-TBI. When investigating the neurodegeneration following TBI, studies have highlighted the role reactive astrocytes have in the neuroinflammation and degeneration process. This review showcases a variety of markers that show reactive astrocyte presence under pathological conditions, including glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3) and S100A10. Astrocyte activation may lead to white-matter inflammation, expressed as white-matter hyperintensities. Other white-matter changes in the brain following TBI include increased cortical thickness in the white matter. This review addresses the gaps in the literature regarding post-mortem human studies focussing on reactive astrocytes, alongside the potential uses of these proteins as markers in the future studies that investigate the proportions of astrocytes in the post-TBI brain has been discussed. This research may benefit future studies that focus on the role reactive astrocytes play in the post-TBI brain and may assist clinicians in managing patients who have suffered TBI.